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Zeitschriftenartikel zum Thema „CCDC80“

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Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 10. März 2023

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1

Liang, Zi-Qian, Li Gao, Jun-Hong Chen, Wen-Bin Dai, Ya-Si Su und Gang Chen. „Downregulation of the Coiled-Coil Domain Containing 80 and Its Perspective Mechanisms in Ovarian Carcinoma: A Comprehensive Study“. International Journal of Genomics 2021 (15.11.2021): 1–20. http://dx.doi.org/10.1155/2021/3752871.

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Introduction. We aimed to explore the downregulation of the coiled-coil domain containing 80 (CCDC80) and its underlying molecular mechanisms in ovarian carcinoma (OVCA). Materials/Methods. Immunohistochemical staining was performed to confirm the expression status of CCDC80 protein. Combining the data from in-house tissue microarrays and high-throughput datasets, we identified the expression level of CCDC80 in OVCA. We utilized cell-type identification by estimating relative subsets of RNA transcripts (CIBERSORT) algorithm and single-sample gene set enrichment analysis (ssGSEA) to explore the relationship between CCDC80 and the tumor microenvironment (TME) landscape in OVCA. Pathway enrichment, function annotation, and transcription factor (TFs) exploration were conducted to study the latent molecular mechanisms. Moreover, the cell line data in the Genomics of Drug Sensitivity in Cancer (GDSC) database was used to discover the relationship between CCDC80 and drug sensitivity. Results. An integrated standard mean difference (SMD) of −0.919 (95% CI: −1.515–0.324, P = 0.002 ) identified the downregulation of CCDC80 in OVCA based on 1048 samples, and the sROC ( AUC = 0.76 ) showed a moderate discriminatory ability of CCDC80 in OVCA. The fraction of infiltrating naive B cells showed significant differences between the high- and low-CCDC80 expression groups. Also, CCDC80-related genes are enriched in the Ras signaling pathway and metabolic of lipid. Nuclear receptor subfamily three group C member 1 (NR3C1) may be an upstream TF of CCDC80, and CCDC80 may be related to the sensitivity of mitocycin C and nilotinib. Conclusion. CCDC80 was downregulated in OVCA and may play a role as a tumor suppressor in OVCA.

2

Grill, Jessica I., und Frank T. Kolligs. „DRO1/CCDC80: a Novel Tumor Suppressor of Colorectal Carcinogenesis“. Current Colorectal Cancer Reports 11, Nr. 4 (19.06.2015): 200–208. http://dx.doi.org/10.1007/s11888-015-0276-3.

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3

Brusegan, Chiara, Anna Pistocchi, Andrea Frassine, Isabella Della Noce, Filippo Schepis und Franco Cotelli. „ccdc80-l1 Is Involved in Axon Pathfinding of Zebrafish Motoneurons“. PLoS ONE 7, Nr. 2 (22.02.2012): e31851. http://dx.doi.org/10.1371/journal.pone.0031851.

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4

Grill, Jessica I., Jens Neumann, Andreas Herbst, Andrea Ofner, Felix Hiltwein, Maximilian K. Marschall, Heike Zierahn, Eckhard Wolf, Marlon R. Schneider und Frank T. Kolligs. „Loss of DRO1/CCDC80 results in obesity and promotes adipocyte differentiation“. Molecular and Cellular Endocrinology 439 (Januar 2017): 286–96. http://dx.doi.org/10.1016/j.mce.2016.09.014.

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5

Leone, Vincenza, Angelo Ferraro, Filippo Schepis, Antonella Federico, Romina Sepe, Claudio Arra, Concetta Langella et al. „The cl2/dro1/ccdc80 null mice develop thyroid and ovarian neoplasias“. Cancer Letters 357, Nr. 2 (Februar 2015): 535–41. http://dx.doi.org/10.1016/j.canlet.2014.12.010.

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6

Tremblay, Frédéric, Tracy Revett, Christine Huard, Ying Zhang, James F. Tobin, Robert V. Martinez und Ruth E. Gimeno. „Bidirectional Modulation of Adipogenesis by the Secreted Protein Ccdc80/DRO1/URB“. Journal of Biological Chemistry 284, Nr. 12 (13.01.2009): 8136–47. http://dx.doi.org/10.1074/jbc.m809535200.

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7

Chan, Siu Chiu, Ying Zhang, Marco Pontoglio und Peter Igarashi. „Hepatocyte nuclear factor-1β regulates Wnt signaling through genome-wide competition with β-catenin/lymphoid enhancer binding factor“. Proceedings of the National Academy of Sciences 116, Nr. 48 (11.11.2019): 24133–42. http://dx.doi.org/10.1073/pnas.1909452116.

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Hepatocyte nuclear factor-1β (HNF-1β) is a tissue-specific transcription factor that is essential for normal kidney development and renal tubular function. Mutations of HNF-1β produce cystic kidney disease, a phenotype associated with deregulation of canonical (β-catenin–dependent) Wnt signaling. Here, we show that ablation of HNF-1β in mIMCD3 renal epithelial cells produces hyperresponsiveness to Wnt ligands and increases expression of Wnt target genes, including Axin2, Ccdc80, and Rnf43. Levels of β-catenin and expression of Wnt target genes are also increased in HNF-1β mutant mouse kidneys. Genome-wide chromatin immunoprecipitation sequencing (ChIP-seq) in wild-type and mutant cells showed that ablation of HNF-1β increases by 6-fold the number of sites on chromatin that are occupied by β-catenin. Remarkably, 50% of the sites that are occupied by β-catenin in HNF-1β mutant cells colocalize with HNF-1β–occupied sites in wild-type cells, indicating widespread reciprocal binding. We found that the Wnt target genes Ccdc80 and Rnf43 contain a composite DNA element comprising a β-catenin/lymphoid enhancer binding factor (LEF) site overlapping with an HNF-1β half-site. HNF-1β and β-catenin/LEF compete for binding to this element, and thereby HNF-1β inhibits β-catenin–dependent transcription. Collectively, these studies reveal a mechanism whereby a transcription factor constrains canonical Wnt signaling through direct inhibition of β-catenin/LEF chromatin binding.

8

Iaccarino, D., M. Fedrigo, C. Castellani, I. Della Noce, S. Carra, F. Cotelli, G. Thiene, A. Angelini und F. Schepis. „P316Expression and functional role of Ccdc80 in developing heart and in cardiomyopathies.“ Cardiovascular Research 103, suppl 1 (27.06.2014): S57.4—S58. http://dx.doi.org/10.1093/cvr/cvu091.4.

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9

O'Leary, Erin E., Anna M. Mazurkiewicz-Muñoz, Lawrence S. Argetsinger, Travis J. Maures, Hung T. Huynh und Christin Carter-Su. „Identification of Steroid-Sensitive Gene-1/Ccdc80 as a JAK2-Binding Protein“. Molecular Endocrinology 27, Nr. 4 (01.04.2013): 619–34. http://dx.doi.org/10.1210/me.2011-1275.

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10

Blanton, Robert M., Craig Cooper, Anja Hergruetter und Timothy Calamaras. „Ccdc80 Functions as a PKGIa Substrate and is Secreted From Cardiac Myocytes“. Journal of Cardiac Failure 23, Nr. 8 (August 2017): S25. http://dx.doi.org/10.1016/j.cardfail.2017.07.064.

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11

Wang, Wei, Congrong Xu, Yan Ren, Shiwei Wang, Chunli Liao, Xiaoyan Fu und Haixia Hu. „A Novel Cancer Stemness-Related Signature for Predicting Prognosis in Patients with Colon Adenocarcinoma“. Stem Cells International 2021 (15.10.2021): 1–23. http://dx.doi.org/10.1155/2021/7036059.

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Objective. To explore the cancer stemness features and develop a novel cancer stemness-related prognostic signature for colon adenocarcinoma (COAD). Methods. We downloaded the mRNA expression data and clinical data of COAD from TCGA database and GEO database. Stemness index, mRNAsi, was utilized to investigate cancer stemness features. Weighted gene coexpression network analysis (WGCNA) was used to identify cancer stemness-related genes. Univariate and multivariate Cox regression analyses were applied to construct a prognostic risk cancer stemness-related signature. We then performed internal and external validation. The relationship between cancer stemness and COAD immune microenvironment was investigated. Results. COAD patients with higher mRNAsi score or EREG-mRNAsi score have significant longer overall survival (OS). We identified 483 differently expressed genes (DEGs) between the high and low mRNAsi score groups. We developed a cancer stemness-related signature using fifteen genes (including RAB31, COL6A3, COL5A2, CCDC80, ADAM12, VGLL3, ECM2, POSTN, DPYSL3, PCDH7, CRISPLD2, COLEC12, NRP2, ISLR, and CCDC8) for prognosis prediction of COAD. Low-risk score was associated with significantly preferable OS in comparison with high-risk score, and the area under the ROC curve (AUC) for OS prediction was 0.705. The prognostic signature was an independent predictor for OS of COAD. Macrophages, mast cells, and T helper cells were the vital infiltration immune cells, and APC costimulation and type II IFN response were the vital immune pathways in COAD. Conclusions. We developed and validated a novel cancer stemness-related prognostic signature for COAD, which would contribute to understanding of molecular mechanism in COAD.

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Osorio-Conles, Óscar, María Guitart, José María Moreno-Navarrete, Xavier Escoté, Xavier Duran, José Manuel Fernandez-Real, Anna María Gómez-Foix, Sonia Fernández-Veledo und Joan Vendrell. „Adipose Tissue and Serum CCDC80 in Obesity and Its Association with Related Metabolic Disease“. Molecular Medicine 23, Nr. 1 (Januar 2017): 225–34. http://dx.doi.org/10.2119/molmed.2017.00067.

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13

Grill, Jessica I., Jens Neumann, Andrea Ofner, Maximilian K. Marschall, Heike Zierahn, Andreas Herbst, Eckhard Wolf und Frank T. Kolligs. „Dro1/Ccdc80 inactivation promotes AOM/DSS-induced colorectal carcinogenesis and aggravates colitis by DSS in mice“. Carcinogenesis 39, Nr. 9 (13.06.2018): 1176–84. http://dx.doi.org/10.1093/carcin/bgy077.

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Fassad, Mahmoud R., Mitali P. Patel, Amelia Shoemark, Thomas Cullup, Jane Hayward, Mellisa Dixon, Andrew V. Rogers et al. „Clinical utility of NGS diagnosis and disease stratification in a multiethnic primary ciliary dyskinesia cohort“. Journal of Medical Genetics 57, Nr. 5 (25.12.2019): 322–30. http://dx.doi.org/10.1136/jmedgenet-2019-106501.

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BackgroundPrimary ciliary dyskinesia (PCD), a genetically heterogeneous condition enriched in some consanguineous populations, results from recessive mutations affecting cilia biogenesis and motility. Currently, diagnosis requires multiple expert tests.MethodsThe diagnostic utility of multigene panel next-generation sequencing (NGS) was evaluated in 161 unrelated families from multiple population ancestries.ResultsMost (82%) families had affected individuals with biallelic or hemizygous (75%) or single (7%) pathogenic causal alleles in known PCD genes. Loss-of-function alleles dominate (73% frameshift, stop-gain, splice site), most (58%) being homozygous, even in non-consanguineous families. Although 57% (88) of the total 155 diagnostic disease variants were novel, recurrent mutations and mutated genes were detected. These differed markedly between white European (52% of families carry DNAH5 or DNAH11 mutations), Arab (42% of families carry CCDC39 or CCDC40 mutations) and South Asian (single LRRC6 or CCDC103 mutations carried in 36% of families) patients, revealing a striking genetic stratification according to population of origin in PCD. Genetics facilitated successful diagnosis of 81% of families with normal or inconclusive ultrastructure and 67% missing prior ultrastructure results.ConclusionsThis study shows the added value of high-throughput targeted NGS in expediting PCD diagnosis. Therefore, there is potential significant patient benefit in wider and/or earlier implementation of genetic screening.

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Raidt, Johanna, Julia Wallmeier, Rim Hjeij, Jörg Große Onnebrink, Petra Pennekamp, Niki T. Loges, Heike Olbrich et al. „Ciliary beat pattern and frequency in genetic variants of primary ciliary dyskinesia“. European Respiratory Journal 44, Nr. 6 (03.09.2014): 1579–88. http://dx.doi.org/10.1183/09031936.00052014.

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Primary ciliary dyskinesia (PCD) is a rare genetic disorder leading to recurrent respiratory tract infections. High-speed video-microscopy analysis (HVMA) of ciliary beating, currently the first-line diagnostic tool for PCD in most centres, is challenging because recent studies have expanded the spectrum of HVMA findings in PCD from grossly abnormal to very subtle. The objective of this study was to describe the diversity of HVMA findings in genetically confirmed PCD individuals.HVMA was performed as part of the routine work-up of individuals with suspected PCD. Subsequent molecular analysis identified biallelic mutations in the PCD-related genes of 66 individuals. 1072 videos of these subjects were assessed for correlation with the genotype.Biallelic mutations (19 novel) were found in 17 genes: DNAI1, DNAI2, DNAH5, DNAH11, CCDC103, ARMC4, KTU/DNAAF2, LRRC50/DNAAF1, LRRC6, DYX1C1, ZMYND10, CCDC39, CCDC40, CCDC164, HYDIN, RSPH4A and RSPH1. Ciliary beat pattern variations correlated well with the genetic findings, allowing the classification of typical HVMA findings for different genetic groups. In contrast, analysis of ciliary beat frequency did not result in additional diagnostic impact.In conclusion, this study provides detailed knowledge about the diversity of HVMA findings in PCD and may therefore be seen as a guide to the improvement of PCD diagnostics.

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Zheng, Mingjun, Heather Mullikin, Anna Hester, Bastian Czogalla, Helene Heidegger, Theresa Vilsmaier, Aurelia Vattai et al. „Development and Validation of a Novel 11-Gene Prognostic Model for Serous Ovarian Carcinomas Based on Lipid Metabolism Expression Profile“. International Journal of Molecular Sciences 21, Nr. 23 (01.12.2020): 9169. http://dx.doi.org/10.3390/ijms21239169.

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(1) Background: Biomarkers might play a significant role in predicting the clinical outcomes of patients with ovarian cancer. By analyzing lipid metabolism genes, future perspectives may be uncovered; (2) Methods: RNA-seq data for serous ovarian cancer were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases. The non-negative matrix factorization package in programming language R was used to classify molecular subtypes of lipid metabolism genes and the limma package in R was performed for functional enrichment analysis. Through lasso regression, we constructed a multi-gene prognosis model; (3) Results: Two molecular subtypes were obtained and an 11-gene signature was constructed (PI3, RGS, ADORA3, CH25H, CCDC80, PTGER3, MATK, KLRB1, CCL19, CXCL9 and CXCL10). Our prognostic model shows a good independent prognostic ability in ovarian cancer. In a nomogram, the predictive efficiency was notably superior to that of traditional clinical features. Related to known models in ovarian cancer with a comparable amount of genes, ours has the highest concordance index; (4) Conclusions: We propose an 11-gene signature prognosis prediction model based on lipid metabolism genes in serous ovarian cancer.

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Zheng, Mingjun, Junyu Long, Anca Chelariu-Raicu, Heather Mullikin, Theresa Vilsmaier, Aurelia Vattai, Helene Hildegard Heidegger et al. „Identification of a Novel Tumor Microenvironment Prognostic Signature for Advanced-Stage Serous Ovarian Cancer“. Cancers 13, Nr. 13 (03.07.2021): 3343. http://dx.doi.org/10.3390/cancers13133343.

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(1) Background: The tumor microenvironment is involved in the growth and proliferation of malignant tumors and in the process of resistance towards systemic and targeted therapies. A correlation between the gene expression profile of the tumor microenvironment and the prognosis of ovarian cancer patients is already known. (2) Methods: Based on data from The Cancer Genome Atlas (379 RNA sequencing samples), we constructed a prognostic 11-gene signature (SNRPA1, CCL19, CXCL11, CDC5L, APCDD1, LPAR2, PI3, PLEKHF1, CCDC80, CPXM1 and CTAG2) for Fédération Internationale de Gynécologie et d’Obstétrique stage III and IV serous ovarian cancer through lasso regression. (3) Results: The established risk score was able to predict the 1-, 3- and 5-year prognoses more accurately than previously known models. (4) Conclusions: We were able to confirm the predictive power of this model when we applied it to cervical and urothelial cancer, supporting its pan-cancer usability. We found that immune checkpoint genes correlate negatively with a higher risk score. Based on this information, we used our risk score to predict the biological response of cancer samples to an anti-programmed death ligand 1 immunotherapy, which could be useful for future clinical studies on immunotherapy in ovarian cancer.

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Jarrin, Miguel, Tanushree Pandit und Lena Gunhaga. „A balance of FGF and BMP signals regulates cell cycle exit and Equarin expression in lens cells“. Molecular Biology of the Cell 23, Nr. 16 (15.08.2012): 3266–74. http://dx.doi.org/10.1091/mbc.e12-01-0075.

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In embryonic and adult lenses, a balance of cell proliferation, cell cycle exit, and differentiation is necessary to maintain physical function. The molecular mechanisms regulating the transition of proliferating lens epithelial cells to differentiated primary lens fiber cells are poorly characterized. To investigate this question, we used gain- and loss-of-function analyses to modulate fibroblast growth factor (FGF) and/or bone morphogenetic protein (BMP) signals in chick lens/retina explants. Here we show that FGF activity plays a key role for proliferation independent of BMP signals. Moreover, a balance of FGF and BMP signals regulates cell cycle exit and the expression of Ccdc80 (also called Equarin), which is expressed at sites where differentiation of lens fiber cells occurs. BMP activity promotes cell cycle exit and induces Equarin expression in an FGF-dependent manner. In contrast, FGF activity is required but not sufficient to induce cell cycle exit or Equarin expression. Furthermore, our results show that in the absence of BMP activity, lens cells have increased cell cycle length or are arrested in the cell cycle, which leads to decreased cell cycle exit. Taken together, these findings suggest that proliferation, cell cycle exit, and early differentiation of primary lens fiber cells are regulated by counterbalancing BMP and FGF signals.

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Della Noce, Isabella, Silvia Carra, Chiara Brusegan, Rosina Critelli, Andrea Frassine, Carlo De Lorenzo, Antonio Giordano et al. „The Coiled-Coil Domain Containing 80 (ccdc80) Gene Regulatesgadd45β2Expression in the Developing Somites of Zebrafish as a New Player of theHedgehogPathway“. Journal of Cellular Physiology 230, Nr. 4 (26.12.2014): 821–30. http://dx.doi.org/10.1002/jcp.24810.

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Terenina, Elena, Stephane Fabre, Agnès Bonnet, Danielle Monniaux, Christèle Robert-Granié, Magali SanCristobal, Julien Sarry et al. „Differentially expressed genes and gene networks involved in pig ovarian follicular atresia“. Physiological Genomics 49, Nr. 2 (01.02.2017): 67–80. http://dx.doi.org/10.1152/physiolgenomics.00069.2016.

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Ovarian folliculogenesis corresponds to the development of follicles leading to either ovulation or degeneration, this latter process being called atresia. Even if atresia involves apoptosis, its mechanism is not well understood. The objective of this study was to analyze global gene expression in pig granulosa cells of ovarian follicles during atresia. The transcriptome analysis was performed on a 9,216 cDNA microarray to identify gene networks and candidate genes involved in pig ovarian follicular atresia. We found 1,684 significantly regulated genes to be differentially regulated between small healthy follicles and small atretic follicles. Among them, 287 genes had a fold-change higher than two between the two follicle groups. Eleven genes ( DKK3, GADD45A, CAMTA2, CCDC80, DAPK2, ECSIT, MSMB, NUPR1, RUNX2, SAMD4A, and ZNF628) having a fold-change higher than five between groups could likely serve as markers of follicular atresia. Moreover, automatic confrontation of deregulated genes with literature data highlighted 93 genes as regulatory candidates of pig granulosa cell atresia. Among these genes known to be inhibitors of apoptosis, stimulators of apoptosis, or tumor suppressors INHBB, HNF4, CLU, different interleukins ( IL5, IL24), TNF-associated receptor ( TNFR1), and cytochrome-c oxidase ( COX) were suggested as playing an important role in porcine atresia. The present study also enlists key upstream regulators in follicle atresia based on our results and on a literature review. The novel gene candidates and gene networks identified in the current study lead to a better understanding of the molecular regulation of ovarian follicular atresia.

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Gong, Duo, Zhen-Wang Zhao, Qiang Zhang, Xiao-hua Yu, Gang Wang, Jin Zou, Xi-long Zheng, Da-wei Zhang, Wei-dong Yin und Chao-ke Tang. „The Long Noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript-1 Regulates CCDC80 Expression by Targeting miR-141-3p/miR-200a-3p in Vascular Smooth Muscle Cells“. Journal of Cardiovascular Pharmacology 75, Nr. 4 (April 2020): 336–43. http://dx.doi.org/10.1097/fjc.0000000000000798.

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Bhatia, Sugandha, Tony Blick, Cletus Pinto, Mark Waltham, James Monkman, Ekaterina Ivanova, Pamela M. Pollock et al. „Identifying Therapies to Combat Epithelial Mesenchymal Plasticity-Associated Chemoresistance to Conventional Breast Cancer Therapies Using An shRNA Library Screen“. Cancers 12, Nr. 5 (30.04.2020): 1123. http://dx.doi.org/10.3390/cancers12051123.

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Background: Breast cancer (BC) is a heterogeneous disease for which the commonly used chemotherapeutic agents primarily include the anthracyclines (doxorubicin, epirubicin), microtubule inhibitors (paclitaxel, docetaxel, eribulin), and alkylating agents (cyclophosphamide). While these drugs can be highly effective, metastatic tumours are frequently refractory to treatment or become resistant upon tumour relapse. Methods: We undertook a cell polarity/epithelial mesenchymal plasticity (EMP)-enriched short hairpin RNA (shRNA) screen in MDA-MB-468 breast cancer cells to identify factors underpinning heterogeneous responses to three chemotherapeutic agents used clinically in breast cancer: Doxorubicin, docetaxel, and eribulin. shRNA-transduced cells were treated for 6 weeks with the EC10 of each drug, and shRNA representation assessed by deep sequencing. We first identified candidate genes with depleted shRNA, implying that their silencing could promote a response. Using the Broad Institute’s Connectivity Map (CMap), we identified partner inhibitors targeting the identified gene families that may induce cell death in combination with doxorubicin, and tested them with all three drug treatments. Results: In total, 259 shRNAs were depleted with doxorubicin treatment (at p < 0.01), 66 with docetaxel, and 25 with eribulin. Twenty-four depleted hairpins overlapped between doxorubicin and docetaxel, and shRNAs for TGFB2, RUNX1, CCDC80, and HYOU1 were depleted across all the three drug treatments. Inhibitors of MDM/TP53, TGFBR, and FGFR were identified by CMap as the top pharmaceutical perturbagens and we validated the combinatorial benefits of the TGFBR inhibitor (SB525334) and MDM inhibitor (RITA) with doxorubicin treatment, and also observed synergy between the inhibitor SB525334 and eribulin in MDA-MB-468 cells. Conclusions: Taken together, a cell polarity/EMP-enriched shRNA library screen identified relevant gene products that could be targeted alongside current chemotherapeutic agents for the treatment of invasive BC.

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Yuan, Hongjun, Qian Yu, Jianyu Pang, Yongzhi Chen, Miaomiao Sheng und Wenru Tang. „The Value of the Stemness Index in Ovarian Cancer Prognosis“. Genes 13, Nr. 6 (31.05.2022): 993. http://dx.doi.org/10.3390/genes13060993.

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Ovarian cancer (OC) is one of the most common gynecological malignancies. It is associated with a difficult diagnosis and poor prognosis. Our study aimed to analyze tumor stemness to determine the prognosis feature of patients with OC. At this job, we selected the gene expression and the clinical profiles of patients with OC in the TCGA database. We calculated the stemness index of each patient using the one-class logistic regression (OCLR) algorithm and performed correlation analysis with immune infiltration. We used consensus clustering methods to classify OC patients into different stemness subtypes and compared the differences in immune infiltration between them. Finally, we established a prognostic signature by Cox and LASSO regression analysis. We found a significant negative correlation between a high stemness index and immune score. Pathway analysis indicated that the differentially expressed genes (DEGs) from the low- and high-mRNAsi groups were enriched in multiple functions and pathways, such as protein digestion and absorption, the PI3K-Akt signaling pathway, and the TGF-β signaling pathway. By consensus cluster analysis, patients with OC were split into two stemness subtypes, with subtype II having a better prognosis and higher immune infiltration. Furthermore, we identified 11 key genes to construct the prognostic signature for patients with OC. Among these genes, the expression levels of nine, including SFRP2, MFAP4, CCDC80, COL16A1, DUSP1, VSTM2L, TGFBI, PXDN, and GAS1, were increased in the high-risk group. The analysis of the KM and ROC curves indicated that this prognostic signature had a great survival prediction ability and could independently predict the prognosis for patients with OC. We established a stemness index-related risk prognostic module for OC, which has prognostic-independent capabilities and is expected to improve the diagnosis and treatment of patients with OC.

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Wang, Xuehua, Wei Liu, Huili Li, Jiaxing Ding, Yu Feng und Zhijian Chen. „Exploring the Role of Obesity in Dilated Cardiomyopathy Based on Bio-informatics Analysis“. Journal of Cardiovascular Development and Disease 9, Nr. 12 (15.12.2022): 462. http://dx.doi.org/10.3390/jcdd9120462.

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(1) Background: Obesity is a major risk factor for cardiovascular disease (CVD), contributing to increasing global disease burdens. Apart from heart failure, coronary artery disease, and arrhythmia, recent research has found that obesity also elevates the risk of dilated cardiomyopathy (DCM). The main purpose of this study was to investigate the underlying biological role of obesity in increasing the risk of DCM. (2) Methods: The datasets GSE120895, GSE19303, and GSE2508 were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were analyzed using GSE120895 for DCM and GSE2508 for obesity, and the findings were compiled to discover the common genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted for the common genes in RStudio. In addition, CIBERSORT was used to obtain the immune cellular composition from DEGs. The key genes were identified in the set of common genes by the least absolute shrinkage and selection operator (LASSO) algorithm, the prognostic risk models of which were verified by receiver operator characteristic (ROC) curves in GSE19303. Finally, Spearman’s correlation was used to explore the connections between key genes and immune cells. (3) Results: GO and KEGG pathway enrichment analyses showed that the main enriched terms of the common genes were transforming growth factor-beta (TGF-β), fibrillar collagen, NADPH oxidase activity, and multiple hormone-related signaling pathways. Both obesity and DCM had a disordered immune environment, especially obesity. The key genes NOX4, CCDC80, COL1A2, HTRA1, and KLHL29 may be primarily responsible for the changes. Spearman’s correlation analysis performed for key genes and immune cells indicated that KLHL29 closely correlated to T cells and M2 macrophages, and HTRA1 very tightly correlated to plasma cells. (4) Conclusions: Bio-informatics analyses performed for DCM and obesity in our study suggested that obesity disturbed the immune micro-environment, promoted oxidative stress, and increased myocardial fibrosis, resulting in ventricular remodeling and an increased risk of DCM. The key genes KLHL29 and HTRA1 may play critical roles in obesity-related DCM.

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Chow, C., N. Wong, M. Pagano, S. W.-M. Lun, K.-I. Nakayama, K. Nakayama und K.-W. Lo. „Regulation of APC/CCdc20 activity by RASSF1A–APC/CCdc20 circuitry“. Oncogene 31, Nr. 15 (29.08.2011): 1975–87. http://dx.doi.org/10.1038/onc.2011.372.

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Hanson, D., P. G. Murray, T. Coulson, A. Sud, A. Omokanye, E. Stratta, F. Sakhinia et al. „Mutations in CUL7, OBSL1 and CCDC8 in 3-M syndrome lead to disordered growth factor signalling“. Journal of Molecular Endocrinology 49, Nr. 3 (27.09.2012): 267–75. http://dx.doi.org/10.1530/jme-12-0034.

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3-M syndrome is a primordial growth disorder caused by mutations in CUL7, OBSL1 or CCDC8. 3-M patients typically have a modest response to GH treatment, but the mechanism is unknown. Our aim was to screen 13 clinically identified 3-M families for mutations, define the status of the GH–IGF axis in 3-M children and using fibroblast cell lines assess signalling responses to GH or IGF1. Eleven CUL7, three OBSL1 and one CCDC8 mutations in nine, three and one families respectively were identified, those with CUL7 mutations being significantly shorter than those with OBSL1 or CCDC8 mutations. The majority of 3-M patients tested had normal peak serum GH and normal/low IGF1. While the generation of IGF binding proteins by 3-M cells was dysregulated, activation of STAT5b and MAPK in response to GH was normal in CUL7−/− cells but reduced in OBSL1−/− and CCDC8−/− cells compared with controls. Activation of AKT to IGF1 was reduced in CUL7−/− and OBSL1−/− cells at 5 min post-stimulation but normal in CCDC8−/− cells. The prevalence of 3-M mutations was 69% CUL7, 23% OBSL1 and 8% CCDC8. The GH–IGF axis evaluation could reflect a degree of GH resistance and/or IGF1 resistance. This is consistent with the signalling data in which the CUL7−/− cells showed impaired IGF1 signalling, CCDC8−/− cells showed impaired GH signalling and the OBSL1−/− cells showed impairment in both pathways. Dysregulation of the GH–IGF–IGF binding protein axis is a feature of 3-M syndrome.

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Vernieri, Claudio, Elena Chiroli, Valentina Francia, Fridolin Gross und Andrea Ciliberto. „Adaptation to the spindle checkpoint is regulated by the interplay between Cdc28/Clbs and PP2ACdc55“. Journal of Cell Biology 202, Nr. 5 (02.09.2013): 765–78. http://dx.doi.org/10.1083/jcb.201303033.

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The spindle checkpoint arrests cells in metaphase until all chromosomes are properly attached to the chromosome segregation machinery. Thereafter, the anaphase promoting complex (APC/C) is activated and chromosome segregation can take place. Cells remain arrested in mitosis for hours in response to checkpoint activation, but not indefinitely. Eventually, they adapt to the checkpoint and proceed along the cell cycle. In yeast, adaptation requires the phosphorylation of APC/C. Here, we show that the protein phosphatase PP2ACdc55 dephosphorylates APC/C, thereby counteracting the activity of the mitotic kinase Cdc28. We also observe that the key regulator of Cdc28, the mitotic cyclin Clb2, increases before cells adapt and is then abruptly degraded at adaptation. Adaptation is highly asynchronous and takes place over a range of several hours. Our data suggest the presence of a double negative loop between PP2ACdc55 and APC/CCdc20 (i.e., a positive feedback loop) that controls APC/CCdc20 activity. The circuit could guarantee sustained APC/CCdc20 activity after Clb2 starts to be degraded.

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Listovsky, Tamar, und Julian E. Sale. „Sequestration of CDH1 by MAD2L2 prevents premature APC/C activation prior to anaphase onset“. Journal of Cell Biology 203, Nr. 1 (07.10.2013): 87–100. http://dx.doi.org/10.1083/jcb.201302060.

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The switch from activation of the anaphase-promoting complex/cyclosome (APC/C) by CDC20 to CDH1 during anaphase is crucial for accurate mitosis. APC/CCDC20 ubiquitinates a limited set of substrates for subsequent degradation, including Cyclin B1 and Securin, whereas APC/CCDH1 has a broader specificity. This switch depends on dephosphorylation of CDH1 and the APC/C, and on the degradation of CDC20. Here we show, in human cells, that the APC/C inhibitor MAD2L2 also contributes to ensuring the sequential activation of the APC/C by CDC20 and CDH1. In prometaphase, MAD2L2 sequestered free CDH1 away from the APC/C. At the onset of anaphase, MAD2L2 was rapidly degraded by APC/CCDC20, releasing CDH1 to activate the dephosphorylated APC/C. Loss of MAD2L2 led to premature association of CDH1 with the APC/C, early destruction of APC/CCDH1 substrates, and accelerated mitosis with frequent mitotic aberrations. Thus, MAD2L2 helps to ensure a robustly bistable switch between APC/CCDC20 and APC/CCDH1 during the metaphase-to-anaphase transition, thereby contributing to mitotic fidelity.

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Fabregat, Matías, Sofía Niño-Rivero, Sabrina Pose, Magdalena Cárdenas-Rodríguez, Mariana Bresque, Karina Hernández, Victoria Prieto-Echagüe et al. „Generation and characterization of Ccdc28b mutant mice links the Bardet-Biedl associated gene with mild social behavioral phenotypes“. PLOS Genetics 18, Nr. 6 (02.06.2022): e1009896. http://dx.doi.org/10.1371/journal.pgen.1009896.

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CCDC28B (coiled-coil domain-containing protein 28B) was identified as a modifier in the ciliopathy Bardet-Biedl syndrome (BBS). Our previous work in cells and zebrafish showed that CCDC28B plays a role regulating cilia length in a mechanism that is not completely understood. Here we report the generation of a Ccdc28b mutant mouse using CRISPR/Cas9 (Ccdc28b mut). Depletion of CCDC28B resulted in a mild phenotype. Ccdc28b mut animals i) do not present clear structural cilia affectation, although we did observe mild defects in cilia density and cilia length in some tissues, ii) reproduce normally, and iii) do not develop retinal degeneration or obesity, two hallmark features of reported BBS murine models. In contrast, Ccdc28b mut mice did show clear social interaction defects as well as stereotypical behaviors. This finding is indeed relevant regarding CCDC28B as a modifier of BBS since behavioral phenotypes have been documented in BBS. Overall, this work reports a novel mouse model that will be key to continue evaluating genetic interactions in BBS, deciphering the contribution of CCDC28B to modulate the presentation of BBS phenotypes. In addition, our data underscores a novel link between CCDC28B and behavioral defects, providing a novel opportunity to further our understanding of the genetic, cellular, and molecular basis of these complex phenotypes.

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Li, Chengliang, Jianjun Mu, Yingpeng Shi und Hong Xin. „LncRNA CCDC26 Interacts with CELF2 Protein to Enhance Myeloid Leukemia Cell Proliferation and Invasion via the circRNA_ANKIB1/miR-195-5p/PRR11 Axis“. Cell Transplantation 30 (01.01.2021): 096368972098608. http://dx.doi.org/10.1177/0963689720986080.

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LncRNA CCDC26 is aberrantly expressed in myeloid leukemia (ML) and promotes myeloid leukemia progression, but the potential mechanism of CCDC26 in regulating ML progression is unclear. In this study, we observed that lncRNA CCDC26 was upregulated in both chronic and acute ML cell lines. LncRNA CCDC26 promoted the proliferation and invasion of K562 and HL-60 cells, which was determined by cell counting kit-8 test and Transwell invasion assay. Flow cytometry showed that lncRNA CCDC26 inhibited cell apoptosis. Bioinformatics and expression correlation analyses revealed that there was a potential interaction between CCDC26 and CUGBP Elav-like family member 2 (CELF2) protein, an RNA bind protein (RBP). Then the relationship between CCDC26 and the RBP CELF2 was identified by using RNA pull-down and RNA immunoprecipitation (RNA-IP) assays. Further analysis showed that overexpression of CCDC26 could noticeably upregulate circRNA_ANKIB1 expression via sponging CELF2. Subsequently, we found that overexpressed circRNA_ANKIB1 could significantly promote proline rich 11 (PRR11) protein expression by sponging miR-195a-5p. Moreover, PRR11 was also upregulated by CCDC26 and downregulated by CELF2. Mechanically, we uncovered that the miR-195a-5p inhibitor activated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways through upregulating PRR11 protein expression. Furthermore, the inhibitors of AKT, p65-NF-κB, or Bcl-2 could inhibit the effect of the miR-195a-5p inhibitor on ML cell behaviors. In conclusion, lncRNA CCDC26 could upregulate PRR11 protein expression by sponging miR-195a-5p, thereby activating the PI3K/AKT and NF-κB pathways to enhance ML cell proliferation and invasion and suppress cell apoptosis.

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Silva, Erica, Ewelina Betleja, Emily John, Philip Spear, James J. Moresco, Siwei Zhang, John R. Yates, Brian J. Mitchell und Moe R. Mahjoub. „Ccdc11 is a novel centriolar satellite protein essential for ciliogenesis and establishment of left–right asymmetry“. Molecular Biology of the Cell 27, Nr. 1 (Januar 2016): 48–63. http://dx.doi.org/10.1091/mbc.e15-07-0474.

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The establishment of left–right (L-R) asymmetry in vertebrates is dependent on the sensory and motile functions of cilia during embryogenesis. Mutations in CCDC11 disrupt L-R asymmetry and cause congenital heart disease in humans, yet the molecular and cellular functions of the protein remain unknown. Here we demonstrate that Ccdc11 is a novel component of centriolar satellites—cytoplasmic granules that serve as recruitment sites for proteins destined for the centrosome and cilium. Ccdc11 interacts with core components of satellites, and its loss disrupts the subcellular organization of satellite proteins and perturbs primary cilium assembly. Ccdc11 colocalizes with satellite proteins in human multiciliated tracheal epithelia, and its loss inhibits motile ciliogenesis. Similarly, depletion of CCDC11 in Xenopus embryos causes defective assembly and motility of cilia in multiciliated epidermal cells. To determine the role of CCDC11 during vertebrate development, we generated mutant alleles in zebrafish. Loss of CCDC11 leads to defective ciliogenesis in the pronephros and within the Kupffer’s vesicle and results in aberrant L-R axis determination. Our results highlight a critical role for Ccdc11 in the assembly and function of motile cilia and implicate centriolar satellite–associated proteins as a new class of proteins in the pathology of L-R patterning and congenital heart disease.

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Liao, Lihong, Hoong-Wei Gan, Vivian Hwa, Mehul Dattani und Andrew Dauber. „Two Siblings with a Mutation in CCDC8 Presenting with Mild Short Stature: A Case of 3-M Syndrome“. Hormone Research in Paediatrics 88, Nr. 5 (2017): 364–70. http://dx.doi.org/10.1159/000477907.

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Background: Short stature can be caused by mutations in a multitude of different genes. 3-M syndrome is a rare growth disorder marked by severe pre- and postnatal growth retardation along with subtle dysmorphic features. There have only been 2 prior reports of mutations in CCDC8 causing 3-M syndrome. Methods: Two patients presenting with mild short stature underwent whole exome sequencing. The mutation was confirmed via Sanger sequencing. We compare the clinical characteristics of our 2 patients to patients previously reported with mutations in the same gene. Results: Exome sequencing identified a homozygous frameshift mutation in CCDC8 in both patients. They presented with a much milder phenotype than previously described patients with the same mutation. Conclusion: In this study, we report a case of 2 sisters with relatively mild short stature who were found via exome sequencing to carry a previously reported homozygous mutation in CCDC8. These patients expand the anthropometric phenotype of 3-M syndrome and demonstrate the power of exome sequencing in the diagnosis of children with short stature. 3-M syndrome should be considered in children with mild skeletal abnormalities, normal/high growth hormone-IGF axis parameters, and normal intelligence.

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Siriphak, Saeranee, Ravinnipa Chanakankun, Tanakorn Proungvitaya, Sittiruk Roytrakul, Doungdean Tummanatsakun, Wunchana Seubwai, Molin Wongwattanakul und Siriporn Proungvitaya. „Kallikrein-11, in Association with Coiled-Coil Domain Containing 25, as a Potential Prognostic Marker for Cholangiocarcinoma with Lymph Node Metastasis“. Molecules 26, Nr. 11 (22.05.2021): 3105. http://dx.doi.org/10.3390/molecules26113105.

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Cholangiocarcinoma (CCA) is a malignancy arising from cholangiocytes. Currently, the treatment and prognosis for CCA are mostly poor. Recently, we have reported that coiled-coil domain containing 25 (CCDC25) protein level in the sera may be a diagnostic marker for CCA. Subsequently, we identified three binding proteins of CCDC25 and found that kallikrein-11 (KLK11) expression was highest among those binding proteins. In this study, we investigated CCDC25 and KLK11 expression in CCA and adjacent normal tissues (n = 18) using immunohistochemistry. The results demonstrated that the expressions of CCDC25 and KLK11 in CCA tissues were both significantly higher than the adjacent tissues (p < 0.001 and p = 0.001, respectively). Then, using GEPIA bioinformatics analysis, KLK11 mRNA was significantly overexpressed in CCA tumor tissues compared with normal tissues (p < 0.05). Moreover, CCDC25 expression was positively correlated with KLK11 expression in CCA with lymph node metastasis (p = 0.028, r = 0.593). An analysis for the interaction of KLK11 with CCDC25 and other proteins, using STRING version 11.0, revealed that CCDC25 and KLK11 correlated with metastasis-related proteins. In addition, Kaplan-Meier survival curve analysis revealed that a high expression of KLK11 was associated with the poor prognosis of CCA. In conclusion, KLK11 is, as a binding protein for CCDC25, possibly involved in the metastatic process of CCA. KLK11 may be used as a prognostic marker for CCA.

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Rishehri, Mehrnoush, Tahereh Etemadi, Leila Pisheh, Ghazaleh Koufigar und Mansoureh Azadeh. „Quantitative Expression of SFN, lncRNA CCDC18-AS1, and lncRNA LINC01343 in Human Breast Cancer as the Regulator Biomarkers in a Novel ceRNA Network: Based on Bioinformatics and Experimental Analyses“. Genetics Research 2022 (12.09.2022): 1–13. http://dx.doi.org/10.1155/2022/6787791.

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Breast cancer (BC) is one of the leading cancers in the world, which has become an increasing serious problem. In this context, reports demonstrate that some long noncoding RNAs (lncRNAs) play significant regulatory roles in breast tumorigenesis and BC progression via various pathways and act as endogenous RNAs. Finding their dysregulation in cancer and evaluating their interaction with other molecules, such as short noncoding RNAs “microRNA (miRNAs)” as well as various genes, are the most important parts in cancer diagnostics. In this study, after performing GSEA and microarray analysis on the GSE71053 dataset, a new ceRNA network of CCDC18-AS1, LINC01343, hsa-miR4462, and SFN in BC was detected by bioinformatics analysis. Therefore, the expression of SFN, CCDC18-AS1, and LINC01343 was quantitatively measured in 24 BC and normal paired tissues using qRT-PCR. CCDC18-AS1, LINC01343, and SFN were expressed higher in BC than in the control (normal paired) tissues based on qRT-PCR data. Furthermore, a significant positive correlation was observed between CCDC18-AS1 and LINC01343 expression in the samples investigated in this study. The investigation of clinicopathological parameters showed that SFN was highly expressed in tumor size of <5 cm and in nonmenopausal ages, while CCDC18-AS1 and LINC01343 indicated a high expression in stages II-III and III of BC, respectively. The overall survival analysis displayed high and low survival in patients with high expression of SFN and CCDC18-AS1, respectively. The ROC curve analysis disclosed that SFN, CCDC18-AS1, and LINC01343 might be suggested as potential biological markers in BC patients. The high expression of CCDC18-AS1, LINC01343, and SFN in BC samples suggests their potential role in BC tumorigenesis and could be considered hallmarks for the diagnosis and prognosis of BC, although this will require further clinical investigations.

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Parsons, S., D. Hall, T. Buggey, A. Holland und P. Verhoeve. „Improving radiation hardness in space-based Charge-Coupled Devices: an experimental validation of a new pre-fabrication modelling technique“. Journal of Instrumentation 17, Nr. 10 (01.10.2022): P10025. http://dx.doi.org/10.1088/1748-0221/17/10/p10025.

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Abstract The soft X-ray imager (SXI) on the SMILE mission uses two large 4510x4510 back illuminated CCD370s to detect X-rays in the 0.2–2 keV range. These devices take heritage from the optical imaging PLATO mission CCD270s and have been optimised for low energy signals by including a parallel supplementary buried channel (SBC) which should reduce the volume of the charge cloud and thereby reduce the number of traps it interacts with as it is transferred through the CCD. The charge transfer performance improvement between the CCD270 and the CCD370 has been simulated using a combination of Silvaco and Matlab models to predict its characteristics pre-fabrication over a 102–105 electron signal range. Trap pumping measurements have been taken on both devices to count the number of traps present and hence calculate the mean amount of traps that exist per pixel across the range of signal levels. The trap pumping results are used to calculate a charge transfer performance improvement that shows good agreement with the simulated values, especially in the SXI science band. These results bring added confidence to the early performance modelling of the SMILE SXI instrument and is a good indicator that the simulations are accurate enough to be used to model devices with more advanced geometries such as an SBC and can be used in future CCD missions, where radiation-hardness and hence good charge transfer characteristics are key.

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Qiao, Renping, Florian Weissmann, Masaya Yamaguchi, Nicholas G. Brown, Ryan VanderLinden, Richard Imre, Marc A. Jarvis et al. „Mechanism of APC/CCDC20 activation by mitotic phosphorylation“. Proceedings of the National Academy of Sciences 113, Nr. 19 (25.04.2016): E2570—E2578. http://dx.doi.org/10.1073/pnas.1604929113.

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Chromosome segregation and mitotic exit are initiated by the 1.2-MDa ubiquitin ligase APC/C (anaphase-promoting complex/cyclosome) and its coactivator CDC20 (cell division cycle 20). To avoid chromosome missegregation, APC/CCDC20 activation is tightly controlled. CDC20 only associates with APC/C in mitosis when APC/C has become phosphorylated and is further inhibited by a mitotic checkpoint complex until all chromosomes are bioriented on the spindle. APC/C contains 14 different types of subunits, most of which are phosphorylated in mitosis on multiple sites. However, it is unknown which of these phospho-sites enable APC/CCDC20 activation and by which mechanism. Here we have identified 68 evolutionarily conserved mitotic phospho-sites on human APC/C bound to CDC20 and have used the biGBac technique to generate 47 APC/C mutants in which either all 68 sites or subsets of them were replaced by nonphosphorylatable or phospho-mimicking residues. The characterization of these complexes in substrate ubiquitination and degradation assays indicates that phosphorylation of an N-terminal loop region in APC1 is sufficient for binding and activation of APC/C by CDC20. Deletion of the N-terminal APC1 loop enables APC/CCDC20 activation in the absence of mitotic phosphorylation or phospho-mimicking mutations. These results indicate that binding of CDC20 to APC/C is normally prevented by an autoinhibitory loop in APC1 and that its mitotic phosphorylation relieves this inhibition. The predicted location of the N-terminal APC1 loop implies that this loop controls interactions between the N-terminal domain of CDC20 and APC1 and APC8. These results reveal how APC/C phosphorylation enables CDC20 to bind and activate the APC/C in mitosis.

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Lu, Dan, Jennifer Y. Hsiao, Norman E. Davey, Vanessa A. Van Voorhis, Scott A. Foster, Chao Tang und David O. Morgan. „Multiple mechanisms determine the order of APC/C substrate degradation in mitosis“. Journal of Cell Biology 207, Nr. 1 (06.10.2014): 23–39. http://dx.doi.org/10.1083/jcb.201402041.

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The ubiquitin protein ligase anaphase-promoting complex or cyclosome (APC/C) controls mitosis by promoting ordered degradation of securin, cyclins, and other proteins. The mechanisms underlying the timing of APC/C substrate degradation are poorly understood. We explored these mechanisms using quantitative fluorescence microscopy of GFP-tagged APC/CCdc20 substrates in living budding yeast cells. Degradation of the S cyclin, Clb5, begins early in mitosis, followed 6 min later by the degradation of securin and Dbf4. Anaphase begins when less than half of securin is degraded. The spindle assembly checkpoint delays the onset of Clb5 degradation but does not influence securin degradation. Early Clb5 degradation depends on its interaction with the Cdk1–Cks1 complex and the presence of a Cdc20-binding “ABBA motif” in its N-terminal region. The degradation of securin and Dbf4 is delayed by Cdk1-dependent phosphorylation near their Cdc20-binding sites. Thus, a remarkably diverse array of mechanisms generates robust ordering of APC/CCdc20 substrate destruction.

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McDonald, Paul C., Wells S. Brown, Zack Gerbec, Shannon Awrey, Joanna Karasinska, David Schaeffer, Daniel Renouf, Ben Stanger und Shoukat Dedhar. „Abstract 5997: The role of neutrophil extracellular trap-CCDC25-integrin linked kinase complex in pancreatic cancer progression and metastasis“. Cancer Research 82, Nr. 12_Supplement (15.06.2022): 5997. http://dx.doi.org/10.1158/1538-7445.am2022-5997.

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Abstract Neutrophils and neutrophil extracellular traps (NETs) contribute to the hypoxic, immunosuppressive pancreatic ductal adenocarcinoma (PDAC) tumour microenvironment (TME) which promotes treatment resistance, increased invasion and metastasis. While recent studies have demonstrated a critical role of tumour cell CCDC25-ILK complex in promoting NET-DNA-induced tumour metastasis in breast cancer, here we have investigated the presence and function of NETosis-induced CCDC25-ILK signaling in the context of pancreatic cancer. We demonstrate that CCDC25 and ILK are expressed in human PDAC cell lines, patient-derived xenograft (PDX) cell lines and in cell lines derived from the KPCY genetic model of PDAC. Importantly, co-immunoprecipitation analyses showed that endogenous CCDC25 and ILK interact in PDAC cells, and the addition of neutrophil-derived NET-DNA resulted in a greater amount of ILK associated with CCDC25 and in increased wound-induced migration. Time-lapse imaging demonstrated a dramatic effect of inhibition of ILK activity on NET-DNA-induced migration by tumour cells in vitro. In vivo, co-localization of CCDC25 and ILK was observed in tumours and liver metastases from both the KPCY GEMM and the MIA PaCa-2 human PDAC xenograft models that were stained by multispectral immunofluorescence for these markers and analyzed by confocal microscopy. Similarly, both tumours and liver metastases showed the presence of infiltrating neutrophils and NETs as indicated by staining for myeloperoxidase and citrullinated histone H3. Collectively, these data identify the neutrophil extracellular trap-induced CCDC25-ILK interaction as an important contributor to PDAC progression and suggest the potential for targeting this axis to prevent NET-induced PDAC progression and metastasis. Citation Format: Paul C. McDonald, Wells S. Brown, Zack Gerbec, Shannon Awrey, Joanna Karasinska, David Schaeffer, Daniel Renouf, Ben Stanger, Shoukat Dedhar. The role of neutrophil extracellular trap-CCDC25-integrin linked kinase complex in pancreatic cancer progression and metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5997.

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Cai, Wei, Meng Wei und Zhen Su. „MITF-Mediated lncRNA CCDC183-As1 Promotes the Tumorigenic Properties and Aerobic Glycolysis of Bladder Cancer via Upregulating TCF7L2“. Journal of Oncology 2022 (31.07.2022): 1–17. http://dx.doi.org/10.1155/2022/6785956.

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As a primary malignancy tumor of the urology system, bladder cancer (BC) is characterized by its high recurrence and metastasis characteristics. Despite the great improvement in clinical interventions over the past decades, the outcomes of BC patients are still unsatisfactory. Novel molecular mechanisms for developing effective diagnostic and therapeutic strategies are urgently needed; therefore, we screened the lncRNA expression profile in four pairs of BC tissues, showing that CCDC183-AS1 was the most upregulated lncRNA. Subsequently, results of CCK-8, EdU, Transwell, and aerobic glycolysis detection showed that CCDC183-AS1 plays an oncogene role in BC progression. Furthermore, an investigation of the downstream and upstream factors of CCDC183-AS1 identified a novel MITF/CCDC183-AS1/miR-4731-5p/TCF7L2 axis in BC progression, which might furnish novel insights for developing effective diagnostic and therapeutic strategies for BC.

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Бочарова, А. В., А. В. Марусин, С. А. Иванова, О. Ю. Федоренко, А. В. Семке und В. А. Степанов. „Genetic variants of the TCF4, LSM1, and CCDC60 genes are associated with schizophrenia“. Nauchno-prakticheskii zhurnal «Medicinskaia genetika», Nr. 4(213) (30.04.2020): 17–19. http://dx.doi.org/10.25557/2073-7998.2020.04.17-19.

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Проведен анализ ассоциаций 30 однонуклеотидных полиморфизмов генов в группах больных шизофренией и контроле общей численностью 1020 образцов ДНК представителей русской популяции Сибирского региона. Для исследования были отобраны маркеры, показавшие ассоциацию с шизофренией или ее когнитивными эндофенотипами в широкогеномных ассоциативных исследованиях. Мультиплексное генотипирование проводилось на платформе «MassARRAY System 4». В результате проведенного анализа выявлены статистически значимые ассоциации, как для аллелей, так и для генотипов полиморфных вариантов генов TCF4, LSM1, CCDC60. Совокупность полученных данных указывает на то, что гены TCF4 и LSM1, вероятно, играют существенную роль в патогенезе шизофрении в популяциях мира. 1020 DNA samples of two groups of people (schizophrenia and control) from the Russian population were analyzed using 30 SNPs. As the analyzed markers, SNPs were selected that showed an association with schizophrenia or variability of cognitive abilities in genome-wide association studies. Multiplex genotyping was performed using the MassARRAY System 4 platform. As a result of the analysis, statistically significant associations were revealed for polymorphic variants of the TCF4, LSM1, CCDC60 genes. Our results confirm the role of the TCF4 and LSM1 genes in the schizophrenia pathogenesis in world populations.

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Clijsters, Linda, Janneke Ogink und Rob Wolthuis. „The spindle checkpoint, APC/CCdc20, and APC/CCdh1 play distinct roles in connecting mitosis to S phase“. Journal of Cell Biology 201, Nr. 7 (17.06.2013): 1013–26. http://dx.doi.org/10.1083/jcb.201211019.

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DNA replication depends on a preceding licensing event by Cdt1 and Cdc6. In animal cells, relicensing after S phase but before mitosis is prevented by the Cdt1 inhibitor geminin and mitotic cyclin activity. Here, we show that geminin, like cyclin B1 and securin, is a bona fide target of the spindle checkpoint and APC/CCdc20. Cyclin B1 and geminin are degraded simultaneously during metaphase, which directs Cdt1 accumulation on segregating sister chromatids. Subsequent activation of APC/CCdh1 leads to degradation of Cdc6 well before Cdt1 becomes unstable in a replication-coupled manner. In mitosis, the spindle checkpoint supports Cdt1 accumulation, which promotes S phase onset. We conclude that the spindle checkpoint, APC/CCdc20, and APC/CCdh1 act successively to ensure that the disappearance of licensing inhibitors coincides exactly with a peak of Cdt1 and Cdc6. Whereas cell cycle entry from quiescence requires Cdc6 resynthesis, our results indicate that proliferating cells use a window of time in mitosis, before Cdc6 is degraded, as an earlier opportunity to direct S phase.

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Hanson, Dan, Adam Stevens, Philip G. Murray, Graeme C. M. Black und Peter E. Clayton. „Identifying biological pathways that underlie primordial short stature using network analysis“. Journal of Molecular Endocrinology 52, Nr. 3 (07.04.2014): 333–44. http://dx.doi.org/10.1530/jme-14-0029.

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Mutations in CUL7, OBSL1 and CCDC8, leading to disordered ubiquitination, cause one of the commonest primordial growth disorders, 3-M syndrome. This condition is associated with i) abnormal p53 function, ii) GH and/or IGF1 resistance, which may relate to failure to recycle signalling molecules, and iii) cellular IGF2 deficiency. However the exact molecular mechanisms that may link these abnormalities generating growth restriction remain undefined. In this study, we have used immunoprecipitation/mass spectrometry and transcriptomic studies to generate a 3-M ‘interactome’, to define key cellular pathways and biological functions associated with growth failure seen in 3-M. We identified 189 proteins which interacted with CUL7, OBSL1 and CCDC8, from which a network including 176 of these proteins was generated. To strengthen the association to 3-M syndrome, these proteins were compared with an inferred network generated from the genes that were differentially expressed in 3-M fibroblasts compared with controls. This resulted in a final 3-M network of 131 proteins, with the most significant biological pathway within the network being mRNA splicing/processing. We have shown using an exogenous insulin receptor (INSR) minigene system that alternative splicing of exon 11 is significantly changed in HEK293 cells with altered expression of CUL7, OBSL1 and CCDC8 and in 3-M fibroblasts. The net result is a reduction in the expression of the mitogenic INSR isoform in 3-M syndrome. From these preliminary data, we hypothesise that disordered ubiquitination could result in aberrant mRNA splicing in 3-M; however, further investigation is required to determine whether this contributes to growth failure.

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Wasserman, Danit, Sapir Nachum, Meital Cohen, Taylor P. Enrico, Meirav Noach-Hirsh, Jasmin Parasol, Sarit Zomer-Polak et al. „Cell cycle oscillators underlying orderly proteolysis of E2F8“. Molecular Biology of the Cell 31, Nr. 8 (01.04.2020): 725–40. http://dx.doi.org/10.1091/mbc.e19-12-0725.

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We uncovered interlocking mechanisms regulating the temporal proteolysis of the transcriptional repressor E2F8 in cycling cells including SCFCyclin F in G2, dephosphorylation of Cdk1 sites, and activation of APC/CCdh1, but not APC/CCdc20 during mitotic exit and G1. Differential stabilization under limited APC/C activity allows E2F8 to reaccumulate during late G1 and coregulate S-phase entry.

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Shi, Xiao, Hao Geng, Hui Yu, Xiaolong Hu, Guanxiong Wang, Jin Yang und Hui Zhao. „Biallelic Variants in CCDC39 Gene Lead to Primary Ciliary Dyskinesia and Kartagener Syndrome“. BioMed Research International 2022 (26.06.2022): 1–8. http://dx.doi.org/10.1155/2022/7130555.

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Background. Primary ciliary dyskinesia (PCD) is a clinical syndrome characterized by cilia with an abnormal structure or function. Its main clinical manifestations comprise chronic bronchitis, cough, recurrent respiratory infections, situs inversus, and male infertility. Single-gene variants are widely assumed to be the main cause of this rare disease, and more than 40 genes have been described to be associated with its onset. CCDC39 is essential for assembling the inner dynein arms and dynein regulatory complex and is important in cilia motility. CCDC39 variants were reported as a monogenic etiology of PCD. Methods. This study investigated two unrelated Chinese patients diagnosed as PCD. The chest computed tomography scan was performed to identify PCD phenotypes of the two probands. Considering the effect of PCD on male fertility, routine semen analysis, sperm morphology examination, and scanning electron microscopy were performed to assess the semen characteristics of male proband in family 2 (F2 II-1), who had a history of infertility. Subsequently, the peripheral blood samples of probands were collected to perform whole-exome sequencing (WES) to explore the possible genetic causes of this disease. Results. Whole-exome sequencing revealed a homozygous CCDC39 variant in the female proband of family 1 (F1 II-1: c.286C>T:p.Arg96Ter) and two compound heterozygous CCDC39 variants in the male proband of family 2 (F2 II-1: c.732_733del: p.Ala245PhefsTer18; c.2800_2802dup:p.Val934dup). The two probands showed the typical PCD phenotypes, including chronic bronchitis, recurrent respiratory infections, and situs inversus. The male proband also showed oligoasthenoteratospermia with multiple morphological abnormalities of the sperm flagella. Additionally, CCDC39 protein level was significantly lower in the sperm of male proband than in the sperm from normal controls. Conclusion. We identified a homozygous variant reported previously and two compound heterozygous variants of CCDC39 possibly responsible for PCD pathogenesis, expanding the variant spectrum of Chinese PCD, Kartagener syndrome, and morphological abnormalities of the sperm flagella involving CCDC39.

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Phillips-Krawczak, Christine A., Amika Singla, Petro Starokadomskyy, Zhihui Deng, Douglas G. Osborne, Haiying Li, Christopher J. Dick et al. „COMMD1 is linked to the WASH complex and regulates endosomal trafficking of the copper transporter ATP7A“. Molecular Biology of the Cell 26, Nr. 1 (Januar 2015): 91–103. http://dx.doi.org/10.1091/mbc.e14-06-1073.

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COMMD1 deficiency results in defective copper homeostasis, but the mechanism for this has remained elusive. Here we report that COMMD1 is directly linked to early endosomes through its interaction with a protein complex containing CCDC22, CCDC93, and C16orf62. This COMMD/CCDC22/CCDC93 (CCC) complex interacts with the multisubunit WASH complex, an evolutionarily conserved system, which is required for endosomal deposition of F-actin and cargo trafficking in conjunction with the retromer. Interactions between the WASH complex subunit FAM21, and the carboxyl-terminal ends of CCDC22 and CCDC93 are responsible for CCC complex recruitment to endosomes. We show that depletion of CCC complex components leads to lack of copper-dependent movement of the copper transporter ATP7A from endosomes, resulting in intracellular copper accumulation and modest alterations in copper homeostasis in humans with CCDC22 mutations. This work provides a mechanistic explanation for the role of COMMD1 in copper homeostasis and uncovers additional genes involved in the regulation of copper transporter recycling.

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Harel, Tamar, John N. Griffin, Thomas Arbogast, Tanner O. Monroe, Flavia Palombo, Marcella Martinelli, Marco Seri, Tommaso Pippucci, Orly Elpeleg und Nicholas Katsanis. „Loss of function mutations in CCDC32 cause a congenital syndrome characterized by craniofacial, cardiac and neurodevelopmental anomalies“. Human Molecular Genetics 29, Nr. 9 (20.04.2020): 1489–97. http://dx.doi.org/10.1093/hmg/ddaa073.

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Abstract Despite the wide use of genomics to investigate the molecular basis of rare congenital malformations, a significant fraction of patients remains bereft of diagnosis. As part of our continuous effort to recruit and perform genomic and functional studies on such cohorts, we investigated the genetic and mechanistic cause of disease in two independent consanguineous families affected by overlapping craniofacial, cardiac, laterality and neurodevelopmental anomalies. Using whole exome sequencing, we identified homozygous frameshift CCDC32 variants in three affected individuals. Functional analysis in a zebrafish model revealed that ccdc32 depletion recapitulates the human phenotypes. Because some of the patient phenotypes overlap defects common to ciliopathies, we asked if loss of CCDC32 might contribute to the dysfunction of this organelle. Consistent with this hypothesis, we show that ccdc32 is required for normal cilia formation in zebrafish embryos and mammalian cell culture, arguing that ciliary defects are at least partially involved in the pathomechanism of this disorder.

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Lara-Gonzalez, Pablo, Taekyung Kim und Arshad Desai. „Taming the Beast: Control of APC/CCdc20-Dependent Destruction“. Cold Spring Harbor Symposia on Quantitative Biology 82 (2017): 111–21. http://dx.doi.org/10.1101/sqb.2017.82.033712.

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Wang, Sheng-Chao, Li-Min Liao, Muhamad Ansar, Shih-Yun Lin, Wei-Wen Hsu, Chih-Ming Su, Yu-Mei Chung, Cai-Cing Liu, Chin-Sheng Hung und Ruo-Kai Lin. „Automatic Detection of the Circulating Cell-Free Methylated DNA Pattern of GCM2, ITPRIPL1 and CCDC181 for Detection of Early Breast Cancer and Surgical Treatment Response“. Cancers 13, Nr. 6 (18.03.2021): 1375. http://dx.doi.org/10.3390/cancers13061375.

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The early detection of cancer can reduce cancer-related mortality. There is no clinically useful noninvasive biomarker for early detection of breast cancer. The aim of this study was to develop accurate and precise early detection biomarkers and a dynamic monitoring system following treatment. We analyzed a genome-wide methylation array in Taiwanese and The Cancer Genome Atlas (TCGA) breast cancer (BC) patients. Most breast cancer-specific circulating methylated CCDC181, GCM2 and ITPRIPL1 biomarkers were found in the plasma. An automatic analysis process of methylated ccfDNA was established. A combined analysis of CCDC181, GCM2 and ITPRIPL1 (CGIm) was performed in R using Recursive Partitioning and Regression Trees to establish a new prediction model. Combined analysis of CCDC181, GCM2 and ITPRIPL1 (CGIm) was found to have a sensitivity level of 97% and an area under the curve (AUC) of 0.955 in the training set, and a sensitivity level of 100% and an AUC of 0.961 in the test set. The circulating methylated CCDC181, GCM2 and ITPRIPL1 was also significantly decreased after surgery (all p < 0.001). The aberrant methylation patterns of the CCDC181, GCM2 and ITPRIPL1 genes means that they are potential biomarkers for the detection of early BC and can be combined with breast imaging data to achieve higher accuracy, sensitivity and specificity, facilitating breast cancer detection. They may also be applied to monitor the surgical treatment response.

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Shoemark, Amelia, Eduardo Moya, Robert A. Hirst, Mitali P. Patel, Evelyn A. Robson, Jane Hayward, Juliet Scully et al. „High prevalence of CCDC103 p.His154Pro mutation causing primary ciliary dyskinesia disrupts protein oligomerisation and is associated with normal diagnostic investigations“. Thorax 73, Nr. 2 (08.08.2017): 157–66. http://dx.doi.org/10.1136/thoraxjnl-2017-209999.

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RationalePrimary ciliary dyskinesia is a genetically heterogeneous inherited condition characterised by progressive lung disease arising from abnormal cilia function. Approximately half of patients have situs inversus. The estimated prevalence of primary ciliary dyskinesia in the UK South Asian population is 1:2265. Early, accurate diagnosis is key to implementing appropriate management but clinical diagnostic tests can be equivocal.ObjectivesTo determine the importance of genetic screening for primary ciliary dyskinesia in a UK South Asian population with a typical clinical phenotype, where standard testing is inconclusive.MethodsNext-generation sequencing was used to screen 86 South Asian patients who had a clinical history consistent with primary ciliary dyskinesia. The effect of a CCDC103 p.His154Pro missense variant compared with other dynein arm-associated gene mutations on diagnostic/phenotypic variability was tested. CCDC103 p.His154Pro variant pathogenicity was assessed by oligomerisation assay.ResultsSixteen of 86 (19%) patients carried a homozygous CCDC103 p.His154Pro mutation which was found to disrupt protein oligomerisation. Variable diagnostic test results were obtained including normal nasal nitric oxide levels, normal ciliary beat pattern and frequency and a spectrum of partial and normal dynein arm retention. Fifteen (94%) patients or their sibling(s) had situs inversus suggesting CCDC103 p.His154Pro patients without situs inversus are missed.ConclusionsThe CCDC103 p.His154Pro mutation is more prevalent than previously thought in the South Asian community and causes primary ciliary dyskinesia that can be difficult to diagnose using pathology-based clinical tests. Genetic testing is critical when there is a strong clinical phenotype with inconclusive standard diagnostic tests.

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Sugrue, Kelsey F., und Irene E. Zohn. „Mechanism for generation of left isomerism in Ccdc40 mutant embryos“. PLOS ONE 12, Nr. 2 (09.02.2017): e0171180. http://dx.doi.org/10.1371/journal.pone.0171180.

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