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Journal articles on the topic 'Cancer cells Breast Genes'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Dai, Xiaofeng, Rong Ma, Xijiang Zhao, and Fengfeng Zhou. "Epigenetic profiles capturing breast cancer stemness for triple negative breast cancer control." Epigenomics 11, no. 16 (2019): 1811–25. http://dx.doi.org/10.2217/epi-2019-0266.

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Aim: Triple-negative breast cancers (TNBCs) contain a higher percentage of breast cancer stem cells (BCSCs) than the other subtypes and lack effective yet safe-targeted therapies. We would like to unveil genes relevant to the therapeutic control of breast cancer stemness at the epigenetic level. Methods: We sequenced the transcriptome of BCSCs isolated from TNBCs, identified genes differentially expressed in these cells and subjected to DNA methylation and established the Bayesian network as well as interactions out of them. Results & conclusion: We presented a core epigenetic BCSC gene pa

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Liu, Li, Yudong Wu, Cheng Zhang, et al. "Cancer-associated adipocyte-derived G-CSF promotes breast cancer malignancy via Stat3 signaling." Journal of Molecular Cell Biology 12, no. 9 (2020): 723–37. http://dx.doi.org/10.1093/jmcb/mjaa016.

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Abstract Adipocyte is the most predominant cell type in the tumor microenvironment of breast cancer and plays a pivotal role in cancer progression, yet the underlying mechanisms and functional mediators remain elusive. We isolated primary preadipocytes from mammary fat pads of human breast cancer patients and generated mature adipocytes and cancer-associated adipocytes (CAAs) in vitro. The CAAs exhibited significantly different gene expression profiles as assessed by transcriptome sequencing. One of the highly expressed genes in CAAs is granulocyte colony-stimulating factor (G-CSF). Treatment

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Hwang-Verslues, Wendy W., King-Jen Chang, Eva Y. H. P. Lee, and Wen-Hwa Lee. "Breast Cancer Stem Cells and Tumor Suppressor Genes." Journal of the Formosan Medical Association 107, no. 10 (2008): 751–66. http://dx.doi.org/10.1016/s0929-6646(08)60188-6.

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Kim, Young-Ho, Hyun-Kyoung Kim, Hee Yeon Kim, et al. "FAK-Copy-Gain Is a Predictive Marker for Sensitivity to FAK Inhibition in Breast Cancer." Cancers 11, no. 9 (2019): 1288. http://dx.doi.org/10.3390/cancers11091288.

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Background: Cancers with copy-gain drug-target genes are excellent candidates for targeted therapy. In order to search for new predictive marker genes, we investigated the correlation between sensitivity to targeted drugs and the copy gain of candidate target genes in NCI-60 cells. Methods: For eight candidate genes showing copy gains in NCI-60 cells identified in our previous study, sensitivity to corresponding target drugs was tested on cells showing copy gains of the candidate genes. Results: Breast cancer cells with Focal Adhesion Kinase (FAK)-copy-gain showed a significantly higher sensit

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Bogacz, Anna, Marlena Wolek, Bogna Juskowiak, et al. "Expression of genes modulated by epigallocatechin-3-gallate in breast cancer cells." Herba Polonica 64, no. 3 (2018): 31–37. http://dx.doi.org/10.2478/hepo-2018-0016.

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Summary Introduction: Breast cancer is the most common malignant cancer among women. Both drug resistance and metastasis are major problems in the treatment of breast cancer. Therefore, adjuvant therapy may improve patients’ survival and affect their quality of life. It is suggested that epigallocatechin gallate (EGCG) which is well known for its chemopreventive activity and acts on numerous molecular targets may inhibit the growth and metastasis of some cancers. Hence, discovering the metastatic molecular mechanisms for breast cancer may be useful for therapy. Objective: The aim of the study

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Zhang, Suping, Han Zhang, Emanuela M. Ghia, et al. "Inhibition of chemotherapy resistant breast cancer stem cells by a ROR1 specific antibody." Proceedings of the National Academy of Sciences 116, no. 4 (2019): 1370–77. http://dx.doi.org/10.1073/pnas.1816262116.

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Breast cancers enduring treatment with chemotherapy may be enriched for cancer stem cells or tumor-initiating cells, which have an enhanced capacity for self-renewal, tumor initiation, and/or metastasis. Breast cancer cells that express the type I tyrosine kinaselike orphan receptor ROR1 also may have such features. Here we find that the expression of ROR1 increased in breast cancer cells following treatment with chemotherapy, which also enhanced expression of genes induced by the activation of Rho-GTPases, Hippo-YAP/TAZ, or B lymphoma Mo-MLV insertion region 1 homolog (BMI1). Expression of RO

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Neiger, Hannah E., Emily L. Siegler, and Yihui Shi. "Breast Cancer Predisposition Genes and Synthetic Lethality." International Journal of Molecular Sciences 22, no. 11 (2021): 5614. http://dx.doi.org/10.3390/ijms22115614.

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BRCA1 and BRCA2 are tumor suppressor genes with pivotal roles in the development of breast and ovarian cancers. These genes are essential for DNA double-strand break repair via homologous recombination (HR), which is a virtually error-free DNA repair mechanism. Following BRCA1 or BRCA2 mutations, HR is compromised, forcing cells to adopt alternative error-prone repair pathways that often result in tumorigenesis. Synthetic lethality refers to cell death caused by simultaneous perturbations of two genes while change of any one of them alone is nonlethal. Therefore, synthetic lethality can be ins

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R., Abhirup H., Priyanka Kenchetty, and Aishwarya K. Chidananda. "Breast ovarian cancer syndrome." International Surgery Journal 8, no. 8 (2021): 2454. http://dx.doi.org/10.18203/2349-2902.isj20213144.

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BRCA1 and BRCA2, known as breast and ovarian cancer predisposition genes, were discovered in the 1990s. As part of a normal genetic structure, these genes are intrinsic to all human beings, but they are mutated in some individuals increasing the risk for breast and ovarian cancers development. BRCA1 is not only expressed in endocrine tissues but is also detected in other cells such as the neuroepithelial cells in the early stage of cell development. Like BRCA1, BRCA2 is also expressed in a wide variety of tissues and is observed with higher rates in the breast and thymus and with lower rates i

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Rossi, Fabiana Alejandra, Ezequiel Hernán Calvo Roitberg, Juliana Haydeé Enriqué Steinberg, Molishree Umesh Joshi, Joaquín Maximiliano Espinosa, and Mario Rossi. "HERC1 Regulates Breast Cancer Cells Migration and Invasion." Cancers 13, no. 6 (2021): 1309. http://dx.doi.org/10.3390/cancers13061309.

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Tumor cell migration and invasion into adjacent tissues is one of the hallmarks of cancer and the first step towards secondary tumors formation, which represents the leading cause of cancer-related deaths. This process is considered an unmet clinical need in the treatment of this disease, particularly in breast cancers characterized by high aggressiveness and metastatic potential. To identify and characterize genes with novel functions as regulators of tumor cell migration and invasion, we performed a genetic loss-of-function screen using a shRNA library directed against the Ubiquitin Proteaso

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Wijshake, Tobias, Zhongju Zou, Beibei Chen, et al. "Tumor-suppressor function of Beclin 1 in breast cancer cells requires E-cadherin." Proceedings of the National Academy of Sciences 118, no. 5 (2021): e2020478118. http://dx.doi.org/10.1073/pnas.2020478118.

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Beclin 1, an autophagy and haploinsufficient tumor-suppressor protein, is frequently monoallelically deleted in breast and ovarian cancers. However, the precise mechanisms by which Beclin 1 inhibits tumor growth remain largely unknown. To address this question, we performed a genome-wide CRISPR/Cas9 screen in MCF7 breast cancer cells to identify genes whose loss of function reverse Beclin 1-dependent inhibition of cellular proliferation. Small guide RNAs targeting CDH1 and CTNNA1, tumor-suppressor genes that encode cadherin/catenin complex members E-cadherin and alpha-catenin, respectively, we

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Liu, Yan, Ai Zhang, Ping-Ping Bao, et al. "MicroRNA-374b inhibits breast cancer progression through regulating CCND1 and TGFA genes." Carcinogenesis 42, no. 4 (2021): 528–36. http://dx.doi.org/10.1093/carcin/bgab005.

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Abstract Emerging evidence indicates that microRNAs (miRNAs) play a critical role in breast cancer development. We recently reported that a higher expression of miR-374b in tumor tissues was associated with a better disease-free survival of triple-negative breast cancer (TNBC). However, the functional significance and molecular mechanisms underlying the role of miR-374b in breast cancer are largely unknown. In this current study, we evaluated the biological functions and potential mechanisms of miR-374b in both TNBC and non-TNBC. We found that miR-374b was significantly downregulated in breast

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Gerashchenko, Tatiana S., Sofia Y. Zolotaryova, Artem M. Kiselev, et al. "The Activity of KIF14, Mieap, and EZR in a New Type of the Invasive Component, Torpedo-Like Structures, Predetermines the Metastatic Potential of Breast Cancer." Cancers 12, no. 7 (2020): 1909. http://dx.doi.org/10.3390/cancers12071909.

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Intratumor morphological heterogeneity reflects patterns of invasive growth and is an indicator of the metastatic potential of breast cancer. In this study, we used this heterogeneity to identify molecules associated with breast cancer invasion and metastasis. The gene expression microarray data were used to identify genes differentially expressed between solid, trabecular, and other morphological arrangements of tumor cells. Immunohistochemistry was applied to evaluate the association of the selected proteins with metastasis. RNA-sequencing was performed to analyze the molecular makeup of met

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Shihab, Israa, Bariaa A. Khalil, Noha Mousaad Elemam, et al. "Understanding the Role of Innate Immune Cells and Identifying Genes in Breast Cancer Microenvironment." Cancers 12, no. 8 (2020): 2226. http://dx.doi.org/10.3390/cancers12082226.

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The innate immune system is the first line of defense against invading pathogens and has a major role in clearing transformed cells, besides its essential role in activating the adaptive immune system. Macrophages, dendritic cells, NK cells, and granulocytes are part of the innate immune system that accumulate in the tumor microenvironment such as breast cancer. These cells induce inflammation in situ by secreting cytokines and chemokines that promote tumor growth and progression, in addition to orchestrating the activities of other immune cells. In breast cancer microenvironment, innate immun

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Wang, Shuning, Xiaoju Li, Wangqian Zhang та ін. "Genome-Wide Investigation of Genes Regulated by ERα in Breast Cancer Cells". Molecules 23, № 10 (2018): 2543. http://dx.doi.org/10.3390/molecules23102543.

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Estrogen receptor alpha (ERα), which has been detected in over 70% of breast cancer cases, is a driving factor for breast cancer growth. For investigating the underlying genes and networks regulated by ERα in breast cancer, RNA-seq was performed between ERα transgenic MDA-MB-231 cells and wild type MDA-MB-231 cells. A total of 267 differentially expressed genes (DEGs) were identified. Then bioinformatics analyses were performed to illustrate the mechanism of ERα. Besides, by comparison of RNA-seq data obtained from MDA-MB-231 cells and microarray dataset obtained from estrogen (E2) stimulated

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JOSEPH JERRY, D., NICHOLAS B. GRINER, and LUWEI TAO. "TUMOR SUPPRESSOR PATHWAYS AND CELLULAR ORIGINS OF BREAST CANCER: NEW COMPLEXITIES AND NEW HOPES." Nano LIFE 01, no. 01n02 (2010): 1–16. http://dx.doi.org/10.1142/s179398441000002x.

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Heritable breast cancer syndromes have identified the recognition and processing of DNA double strand breaks as a fundamental vulnerability in the breast epithelium. The role of homology-directed DNA repair is particularly prominent, indicating that this repair pathway is rate-limiting. Although the activities of the tumor suppressor genes underlying heritable breast cancer act in a common pathway of DNA double strand break repair, the specific lesions result in surprisingly different patterns of biomarkers in the breast cancers, suggesting that they arise from different cell types that includ

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Sharma, D., B. B. Knight, R. Yacoub, et al. "Using epigenetic reprogramming to target triple-negative breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (2009): e14565-e14565. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14565.

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e14565 Background: The outcome for patients with breast cancer has been significantly improved by the use of targeted agents. The prognosis of triple negative (TN) breast cancers, which do not express hormone receptors (ER, PR) or Her2, is poor, because of an aggressive clinical course and lack of targeted therapeutic agents. Epigenetic silencing of specific genes has been observed in breast cancer and some of these genes are more important due to available targeted therapies such as ER. Since all endocrine therapies are designed to block ER function in some way, the identification of new ther

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Karami, Faezeh, Narges Maleki, Arefeh Khazraei Monfared, and Sayeh Jafari Marandi. "Upregulation of miR-206 is a potential diagnostic biomarker in breast cancer." Bionatura 6, no. 2 (2021): 1757–62. http://dx.doi.org/10.21931/rb/2021.06.02.15.

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Breast cancer is one of the most common malignancies, and like most cancers, most cases are caused by somatic mutations. Due to estrogen's role in the growth, differentiation, and division of breast and endometrial cancer cells, tamoxifen is used as an estrogen receptor antagonist in breast cancer cells with estrogen receptor (ER +) has a special place, which unfortunately in one-third of the Cases are resisted. This study aimed to investigate the effect of tamoxifen-treated tumor-derived exosomes on the expression pattern of Twist and Bcl-2 oncogenic genes in fibroblast cells. MCF-7 breast ca

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Kocemba-Pilarczyk, Kinga A., Paulina Dudzik, and Katarzyna Leśkiewicz. "The relationship between expression of VIMENTIN and CD146 genes in breast cancer." Bio-Algorithms and Med-Systems 17, no. 1 (2021): 1–7. http://dx.doi.org/10.1515/bams-2020-0058.

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Abstract Objectives CD146 is an adhesive molecule that was originally reported on malignant melanoma cells as a protein crucial for cell adhesion. It is now known that high expression of the CD146 protein is not only characteristic of melanoma, but it occurs on a number of cancers, contributing to worse prognosis and increased aggressiveness. Independent in vitro studies in breast cancer have shown that CD146 protein alone can induce a change in epithelial to mesenchymal transcriptional profile, which is the basis of the tumor aggressiveness and metastasis. Methods In the following work, the c

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Inoue, A., N. Yoshida, Y. Omoto, et al. "Development of cDNA microarray for expression profiling of estrogen-responsive genes." Journal of Molecular Endocrinology 29, no. 2 (2002): 175–92. http://dx.doi.org/10.1677/jme.0.0290175.

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Estrogen plays an important role in many physiological events including carcinogenesis and the development of human breast cancer. However, the molecular mechanisms of estrogen signaling in cancers have not been clarified hitherto and accurate therapeutic prediction of breast cancer is earnestly desired. We first carried out estrogen-responsive expression profiling of approximately 9000 genes in estrogen receptor-positive human MCF-7 breast cancer cells. Based on the results, estrogen-responsive genes were selected for production of a custom-made cDNA microarray. Using a microarray consisting

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Ward, Ashley Vanessa, Shawna B. Matthews, and Carol A. Sartorius. "3300 Progesterone receptor alters lipid biology in luminal breast cancer." Journal of Clinical and Translational Science 3, s1 (2019): 19. http://dx.doi.org/10.1017/cts.2019.46.

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OBJECTIVES/SPECIFIC AIMS: These studies seek to evaluate hormonal regulation of luminal breast cancer lipid metabolism and to identify targetable progesterone-mediated changes in lipid biology that contribute to therapeutic resistance in breast cancer. METHODS/STUDY POPULATION: Established and patient-derived luminal breast cancer cell lines, which express ER and PR, were used for this study. RNA transcript and protein expression levels were evaluated by qRT-PCR and immunoblot, respectively. Broad scale lipidomics of progesterone-treated cells was conducted via ultra-high pressure liquid chrom

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Cobleigh, Melody A., Molly DiScala, Matthew S. Najor, Timothy Yung, and Abde M. Abukhdeir. "STAT6 expression and trastuzumab resistance in HER2+ breast cancer." Journal of Clinical Oncology 38, no. 15_suppl (2020): e13006-e13006. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e13006.

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e13006 Background: Approximately 20% of breast cancers are HER2-positive. Trastuzumab has improved patient outcomes significantly for these cancers. However, acquired resistance occurs in almost all patients with metastatic breast cancer. Therefore, identifying molecular changes that are associated with trastuzumab resistance is worthwhile. STAT6 is a transcription factor that regulates a variety of genes involved in cell cycle regulation, growth inhibition, and apoptosis. STAT6 expression is lost in approximately 3% of breast cancers, but little work has been done in the context of trastuzuma

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Chen, Yongqiang, Ruobing Wang, Shujun Huang, Elizabeth S. Henson, Jayce Bi, and Spencer B. Gibson. "Erb-b2 Receptor Tyrosine Kinase 2 (ERBB2) Promotes ATG12-Dependent Autophagy Contributing to Treatment Resistance of Breast Cancer Cells." Cancers 13, no. 5 (2021): 1038. http://dx.doi.org/10.3390/cancers13051038.

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The epidermal growth factor receptor (EGFR) family member erb-b2 receptor tyrosine kinase 2 (ERBB2) is overexpressed in many types of cancers leading to (radio- and chemotherapy) treatment resistance, whereas the underlying mechanisms are still unclear. Autophagy is known to contribute to cancer treatment resistance. In this study, we demonstrate that ERBB2 increases the expression of different autophagy genes including ATG12 (autophagy-related 12) and promotes ATG12-dependent autophagy. We clarify that lapatinib, a dual inhibitor for EGFR and ERBB2, promoted autophagy in cells expressing only

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El-Masry, Omar S., Arafat Goja, Mostafa Rateb, Amani Y. Owaidah, and Khaldoon Alsamman. "RNA sequencing identified novel target genes for Adansonia digitata in breast and colon cancer cells." Science Progress 104, no. 3 (2021): 003685042110320. http://dx.doi.org/10.1177/00368504211032084.

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Adansonia digitata exhibits numerous beneficial effects. In the current study, we investigated the anti-cancer effects of four different extracts of A. digitata (polar and non-polar extracts of fruit powder and fibers) on the proliferation of human colon cancer (HCT116), human breast cancer (MCF-7), and human ovarian cancer (OVCAR-3 and OVCAR-4) cell lines. RNA sequencing revealed the influence of the effective A. digitata fraction on the gene expression profiles of responsive cells. The results indicated that only the polar extract of the A. digitata fibers exhibited anti-proliferative activi

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Atalay, Arzu, Tim Crook, Mehmet Ozturk, and Isik G. Yulug. "Identification of genes induced by BRCA1 in breast cancer cells." Biochemical and Biophysical Research Communications 299, no. 5 (2002): 839–46. http://dx.doi.org/10.1016/s0006-291x(02)02751-1.

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Meech, Robyn, Dong Gui Hu, Apichaya Chanawong, et al. "Regulation of UDP glucuronosyltransferase 2B genes in breast cancer cells." Drug Metabolism and Pharmacokinetics 33, no. 1 (2018): S55. http://dx.doi.org/10.1016/j.dmpk.2017.11.188.

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Yunita, Elvira. "Epigenetic Regulation of Breast Cancer Stem Cells." Biomedical Journal of Indonesia 7, no. 2 (2021): 270–84. http://dx.doi.org/10.32539/bji.v7i2.289.

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Breast cancer arises as a result of abnormal breast cells forming at an uncontrolled rate. Death in this case of breast cancer is due to the ability of cancer cells to adapt so that it can have an effect on metastasis and recurrence of cancer that was previously thought to have been resolved. The results showed, there is a stem cell population in breast cancer cases which will cause breast cancer to become increasingly difficult to treat. Such cells are known as breast cancer stem cells.Breast cancer cells have the ability to differentiate and contribute greatly to the breast cancer program, a

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Shirkavand, Atefeh, Zahra N. Boroujeni, and Seyed A. Aleyasin. "Solanum nigrum Anticancer Effect Through Epigenetic Modulations in Breast Cancer Cell Lines." Current Cancer Therapy Reviews 16, no. 2 (2020): 121–26. http://dx.doi.org/10.2174/1573394715666190101114541.

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Background: DNA methylation plays an important role in the regulation of gene expression in mammalian cells and often occurs at CpG islands in the genome. It is more reversible than genetic variations and has therefore attracted much attention for the treatment of many diseases, especially cancer. In the present study, we investigated the effect of Solanum nigrum Extract (SNE) on the methylation status of the VIM and CXCR4 genes in breast cancer cell lines. Methods: The Trypan blue assay was used to study the effect of SNE at various concentrations of 0, 0.1, 1.5, 2.5, 3.5 and 5 mg/ml for 48 h

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Eiro, Noemi, Sandra Cid, Nuria Aguado, et al. "MMP1 and MMP11 Expression in Peripheral Blood Mononuclear Cells upon Their Interaction with Breast Cancer Cells and Fibroblasts." International Journal of Molecular Sciences 22, no. 1 (2020): 371. http://dx.doi.org/10.3390/ijms22010371.

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Tumor-infiltrating immune cells phenotype is associated with tumor progression. However, little is known about the phenotype of the peripheral blood mononuclear cells (PBMC) from breast cancer patients. We investigated MMP1 and MMP11 expression in PBMC from breast cancer patients and we analyzed gene expression changes upon their interaction with cancer cells and cancer-associated fibroblasts (CAF). We measured the impact of PBMC on proinflammatory gene expression in breast cancer cells, normal fibroblast (NF), and CAF and the impact on proliferation and invasiveness capacity of breast cancer

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Ying, Xuexiang, Yunpo Sun, and Pingqing He. "Bone Morphogenetic Protein-7 Inhibits EMT-Associated Genes in Breast Cancer." Cellular Physiology and Biochemistry 37, no. 4 (2015): 1271–78. http://dx.doi.org/10.1159/000430249.

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Background/Aims: Bone morphogenetic protein-7 (BMP7) has been shown to reduce the severity of injury-induced fibrosis through counteracting the fibrotic effects of transforming growth factor β 1 (TGFβ1). However, this model in the carcinogenesis of breast cancer is unknown. Methods: We analyzed the effects of BMP7 and TGFβ1 on gene transcripts and protein levels of EMT-related factors in breast cancer cells by RT-qPCR and Western blot, respectively. The effects of BMP7 and TGFβ1 on cell invasiveness and migration were evaluated by scratch wound healing assay and transwell cell migration assay.

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Zhang, F., Y. Xu, C. Song, et al. "Regulational effects of breast cancer stromal cells and normal breast stromal cells on MCF-7 mammosphere formation." Journal of Clinical Oncology 27, no. 15_suppl (2009): 1056. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.1056.

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1056 Background: It is well known that microenvironment plays an important role in tumor progression so we investigated the regulatory effects of breast cancer stromal cells (BCSCs) and normal breast stromal cells (NBSCs) as microenvironment on MCF-7 mammosphere formation. Methods: MCF-7 cells were cultured in suspension to generate mammospheres. The proportion of CD44+CD24- cells was assessed by flow cytometry and the expression of Wint1, notch1, β-catenin, CXCR4, SOX2, and ALDH3A1 was detected by real-time PCR. The stromal cells were purified and identified by immumohistochemistry. BCSCs or

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Chu, Pei-Yi, Ming-Feng Hou, Ji-Ching Lai, Long-Fong Chen, and Chang-Shen Lin. "Cell Reprogramming in Tumorigenesis and Its Therapeutic Implications for Breast Cancer." International Journal of Molecular Sciences 20, no. 8 (2019): 1827. http://dx.doi.org/10.3390/ijms20081827.

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Breast cancer is the most common malignancy in women worldwide and can be categorized into several subtypes according to histopathological parameters or genomic signatures. Such heterogeneity of breast cancer can arise from the reactivation of mammary stem cells in situ during tumorigenesis. Moreover, different breast cancer subtypes exhibit varieties of cancer incidence, therapeutic response, and patient prognosis, suggesting that a specific therapeutic protocol is required for each breast cancer subtype. Recent studies using molecular and cellular assays identified a link between specific ge

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Lu, Xiangdong, Jingjing Ma, Jiahui Chu, et al. "MiR-129-5p Sensitizes the Response of Her-2 Positive Breast Cancer to Trastuzumab by Reducing Rps6." Cellular Physiology and Biochemistry 44, no. 6 (2017): 2346–56. http://dx.doi.org/10.1159/000486122.

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Background/Aims: Trastuzumab is an important treatment used for patients with Her-2-positive breast cancer, but an increasing incidence of trastuzumab resistance has been observed clinically during the past decade. Aberrant microRNA (miR) expression levels are correlated with prognosis and response to trastuzumab in breast cancer. MiR-129-5p is downregulated in trastuzumab-resistant human breast cancer cells (JIMT-1), but its potential function and underlying mechanism remain unclear. Methods: Quantitative RT-PCR (qRT-PCR) was used to determine the expression levels of miR-129-5p and its poten

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Post, Annemarie E. M., Johan Bussink, Fred C. G. J. Sweep, and Paul N. Span. "Changes in DNA Damage Repair Gene Expression and Cell Cycle Gene Expression Do Not Explain Radioresistance in Tamoxifen-Resistant Breast Cancer." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 28, no. 1 (2020): 33–40. http://dx.doi.org/10.3727/096504019x15555794826018.

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Tamoxifen-induced radioresistance, reported in vitro, might pose a problem for patients who receive neoadjuvant tamoxifen treatment and subsequently receive radiotherapy after surgery. Previous studies suggested that DNA damage repair or cell cycle genes are involved, and could therefore be targeted to preclude the occurrence of cross-resistance. We aimed to characterize the observed cross-resistance by investigating gene expression of DNA damage repair genes and cell cycle genes in estrogen receptor-positive MCF-7 breast cancer cells that were cultured to tamoxifen resistance. RNA sequencing

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Dharmarajan, A., N. Zeps, and S. McLaren. "003.Expression of secreted frizzled related protein-4 (sFRP-4) and associated Wnt signalling in cancer and apoptosis." Reproduction, Fertility and Development 17, no. 9 (2005): 63. http://dx.doi.org/10.1071/srb05abs003.

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We examined the interplay between Wnt and secreted frizzled related protein-4 (sFRP4) in estradiol induced cell growth in breast cancer cells (MCF-7), and also determined the in vivo distribution of sFRP-4 in human breast cancer. MCF-7 cells were treated with estradiol, sFRP-4 conditioned media and a combination of the two. Real-time RT-PCR and Western blot analysis were used to determine the expression of the sFRP-4 and its associated Wnt signalling molecules following treatment. Immunohistochemistry was performed to examine sFRP-4 expression patterns in human breast cancers. Estradiol treatm

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Chimonidou, Maria, Areti Strati, Alexandra Tzitzira, et al. "DNA Methylation of Tumor Suppressor and Metastasis Suppressor Genes in Circulating Tumor Cells." Clinical Chemistry 57, no. 8 (2011): 1169–77. http://dx.doi.org/10.1373/clinchem.2011.165902.

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BACKGROUND Circulating tumor cells (CTCs) are associated with prognosis in a variety of human cancers and have been proposed as a liquid biopsy for follow-up examinations. We show that tumor suppressor and metastasis suppressor genes are epigenetically silenced in CTCs isolated from peripheral blood of breast cancer patients. METHODS We obtained peripheral blood from 56 patients with operable breast cancer, 27 patients with verified metastasis, and 23 healthy individuals. We tested DNA extracted from the EpCAM-positive immunomagnetically selected CTC fraction for the presence of methylated and

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Park, Yun-Yong, Sung Yun Jung, Nicholas B. Jennings, et al. "FOXM1 mediates Dox resistance in breast cancer by enhancing DNA repair." Carcinogenesis 33, no. 10 (2012): 1843–53. http://dx.doi.org/10.1093/carcin/bgs167.

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Abstract Transcription factors are direct effectors of altered signaling pathways in cancer and frequently determine clinical outcomes in cancer patients. To uncover new transcription factors that would determine clinical outcomes in breast cancer, we systematically analyzed gene expression data from breast cancer patients. Our results revealed that Forkhead box protein M1 (FOXM1) is the top-ranked survival-associated transcription factor in patients with triple-negative breast cancer. Surprisingly, silencing FOXM1 expression led breast cancer cells to become more sensitive to doxorubicin (Dox

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Lorico, Aurelio, and Germana Rappa. "Phenotypic Heterogeneity of Breast Cancer Stem Cells." Journal of Oncology 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/135039.

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Many types of tumors are organized in a hierarchy of heterogeneous cell populations, with only a small proportion of cancer stem cells (CSCs) capable of sustaining tumor formation and growth, giving rise to differentiated cells, which form the bulk of the tumor. Proof of the existence of CSC comes from clinical experience with germ-cell cancers, where the elimination of a subset of undifferentiated cells can cure patients (Horwich et al., 2006), and from the study of leukemic cells (Bonnet and Dick, 1997; Lapidot et al., 1994; and Yilmaz et al., 2006). The discovery of CSC in leukemias as well

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Xiang, S., L. Mao, T. Duplessis, et al. "Oscillation of Clock and Clock Controlled Genes Induced by Serum Shock in Human Breast Epithelial and Breast Cancer Cells: Regulation by Melatonin." Breast Cancer: Basic and Clinical Research 6 (January 2012): BCBCR.S9673. http://dx.doi.org/10.4137/bcbcr.s9673.

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This study investigates differences in expression of clock and clock-controlled genes (CCGs) between human breast epithelial and breast cancer cells and breast tumor xenografts in circadian intact rats and examines if the pineal hormone melatonin influences clock gene and CCG expression. Oscillation of clock gene expression was not observed under standard growth conditions in vitro, however, serum shock (50% horse serum for 2 h) induced oscillation of clock gene and CCG expression in MCF-10A cells, which was repressed or disrupted in MCF-7 cells. Melatonin administration following serum shock

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Shiu, Li Yen, Chia Hua Liang, Li Ching Chang, Hamm Ming Sheu, Eing Mei Tsai, and Kou Wha Kuo. "Solamargine induces apoptosis and enhances susceptibility to trastuzumab and epirubicin in breast cancer cells with low or high expression levels of HER2/neu." Bioscience Reports 29, no. 1 (2008): 35–45. http://dx.doi.org/10.1042/bsr20080028.

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Trastuzumab is used for breast cancer patients with high expression levels of HER2 (human epidermal growth factor receptor 2)/neu; however, it has no effect on cancers with low levels of HER2/neu. SM (solamargine), a major steroidal alkaloid glycoside purified from Solanum incanum, triggered apoptosis of breast cancer cells (MCF-7 and SK-BR-3 cells) and non-cancerous breast epithelial cells (HBL-100 cells) within 3 h. To extend the application of trastuzumab in breast cancer patients, the regulation of HER2/neu expression by SM was investigated. SM significantly up-regulates HER2/neu expressio

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Chuffa, Luiz Gustavo de Almeida, Fábio Rodrigues Ferreira Seiva, Maira Smaniotto Cucielo, Henrique Spaulonci Silveira, Russel J. Reiter, and Luiz Antonio Lupi. "Clock genes and the role of melatonin in cancer cells: an overview." Melatonin Research 2, no. 2 (2019): 133–57. http://dx.doi.org/10.32794/mr11250026.

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Circadian rhythms control most biological processes in every organism and their disruption or an aberrant function in the expression of clock genes are associated with a number of cancers including some hormone-dependent and independent cancers. The processes involved in carcinogenesis and tumor progression are complex, but understanding the daily profiles of the core clock genes and their clock-controlled genes is essential to evaluate specifically the molecular program of the cancer phenotype; this may be helpful in providing a more realistic strategy for both diagnosis and treatment during

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Cichon, Magdalena A., Celeste M. Nelson, and Derek C. Radisky. "Regulation of Epithelial-Mesenchymal Transition in Breast Cancer Cells by Cell Contact and Adhesion." Cancer Informatics 14s3 (January 2015): CIN.S18965. http://dx.doi.org/10.4137/cin.s18965.

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Epithelial-mesenchymal transition (EMT) is a physiological program that is activated during cancer cell invasion and metastasis. We show here that EMT-related processes are linked to a broad and conserved program of transcriptional alterations that are influenced by cell contact and adhesion. Using cultured human breast cancer and mouse mammary epithelial cells, we find that reduced cell density, conditions under which cell contact is reduced, leads to reduced expression of genes associated with mammary epithelial cell differentiation and increased expression of genes associated with breast ca

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Meaburn, Karen J., Prabhakar R. Gudla, Sameena Khan, Stephen J. Lockett, and Tom Misteli. "Disease-specific gene repositioning in breast cancer." Journal of Cell Biology 187, no. 6 (2009): 801–12. http://dx.doi.org/10.1083/jcb.200909127.

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Genomes are nonrandomly organized within the three-dimensional space of the cell nucleus. Here, we have identified several genes whose nuclear positions are altered in human invasive breast cancer compared with normal breast tissue. The changes in positioning are gene specific and are not a reflection of genomic instability within the cancer tissue. Repositioning events are specific to cancer and do not generally occur in noncancerous breast disease. Moreover, we show that the spatial positions of genes are highly consistent between individuals. Our data indicate that cancer cells have disease

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Mishra, Akanksha, Maria Bonello, Adam Byron, Simon P. Langdon, and Andrew H. Sims. "Evaluation of Gene Expression Data From Cybrids and Tumours Highlights Elevated NDRG1-Driven Proliferation in Triple-Negative Breast Cancer." Breast Cancer: Basic and Clinical Research 14 (January 2020): 117822342093444. http://dx.doi.org/10.1177/1178223420934447.

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Background: Triple-negative breast cancer is an aggressive type of breast cancer with high risk of recurrence. It is still poorly understood and lacks any targeted therapy, which makes it difficult to treat. Thus, it is important to understand the underlying mechanisms and pathways that are dysregulated in triple-negative breast cancer. Methods: To investigate the role of mitochondria in triple-negative breast cancer progression, we analysed previously reported gene expression data from triple-negative breast cancer cybrids with SUM-159 as the nuclear donor cell and SUM-159 or A1N4 (c-SUM-159,

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Shi, Ying, Weihua Gong, Xiangrong Gong, Ping Wang, and Xin Zhao. "Genome-wide DNA methylation analysis of breast cancer MCF-7 / Taxol cells with MeDIP-Seq." PLOS ONE 15, no. 12 (2020): e0241515. http://dx.doi.org/10.1371/journal.pone.0241515.

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Breast cancer (BC) is the most frequently diagnosed tumor in women worldwide. Although the combination of surgery and Taxol chemotherapy can achieve a certain therapeutic effect, patients often develop drug-resistance, resulting in a poor prognosis. Therefore, it is significative to seek the molecular mechanism of chemotherapy resistance. Recent studies have found that abnormal epigenetic regulation in breast cells changes the expression of key genes, which can lead to the occurrence, development, and maintenance of cancer, even related to the development of drug-resistance. Therefore, in this

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Kuroiwa, Yuka, Jun Nakayama, Chihiro Adachi, Takafumi Inoue, Shinya Watanabe, and Kentaro Semba. "Proliferative Classification of Intracranially Injected HER2-positive Breast Cancer Cell Lines." Cancers 12, no. 7 (2020): 1811. http://dx.doi.org/10.3390/cancers12071811.

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HER2 is overexpressed in 25–30% of breast cancers, and approximately 30% of HER2-positive breast cancers metastasize to the brain. Although the incidence of brain metastasis in HER2-positive breast cancer is high, previous studies have been mainly based on cell lines of the triple-negative subtype, and the molecular mechanisms of brain metastasis in HER2-positive breast cancer are unclear. In the present study, we performed intracranial injection using nine HER2-positive breast cancer cell lines to evaluate their proliferative activity in brain tissue. Our results show that UACC-893 and MDA-MB

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Singer, C. F., D. Gschwantler-Kaulich, A. Fink-Retter, et al. "Differential gene expression profile in breast cancer-derived stromal fibroblasts." Journal of Clinical Oncology 25, no. 18_suppl (2007): 21075. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21075.

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21075 Background: Breast cancer is chatacterized by malignant transformation of epithelial cells, but stromal cells also play an important role in tumorigenesis. While tumoral fibroblasts display unique phenotypical properties, it is unclear whether they also represent are a specific subpopulation. Materials and Methods: Stromal fibroblasts deriving from malignant tissue of 10 women with invasive breast cancer, and from normal breast tissue of 10 women with benign breast disorders, were subjected to differential complementary DNA Microarray Analysis by using a 2400 gene cDNA array. Gene expres

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Desestret, V., D. Pissaloux, I. Treilleux, et al. "JS1.1 Specific genetic alterations of breast tumors lead to Yo paraneoplastic cerebellar syndromes." Neuro-Oncology 21, Supplement_3 (2019): iii4. http://dx.doi.org/10.1093/neuonc/noz126.010.

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Abstract BACKGROUND Paraneoplastic cerebellar degenerations with anti-Yo antibodies (Yo-PCD) are rare syndromes associated with ovarian or breast cancers and caused by an auto-immune response against neuronal antigens expressed by tumor cells. We previously demonstrated in Yo-PCD ovarian cancers an association between massive infiltration of ovarian tumors by activated immune effector cells and recurrent gains and/or mutations of onconeural Yo genes (CDR2L and CDR2), suggesting that such genetic alterations in ovarian tumor cells may trigger immune tolerance breakdown and initiation of the aut

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Ansari, Narges, Saeid Shahrabi, Abbas Khosravi, Reza Shirzad, and Hadi Rezaeean. "Prognostic Significance of CHEK2 Mutation in Progression of Breast Cancer." Laboratory Medicine 50, no. 3 (2019): e36-e41. http://dx.doi.org/10.1093/labmed/lmz009.

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Abstract Breast cancer (BC) is one of the most common cancers among women; genetic mutations reflect the development of this disease. Mutations in cell signaling factors can be the main cause of BC development. In this study, we focused on mutations in checkpoint kinase 2 (CHEK2) and their impact as a prognostic factor in the pathogenesis of BC. CHEK2 is controlled in cell signaling pathways through the influence of upstream genes. Also, several downstream genes are regulated by CHEK2. In addition, mutations in CHEK2 lead to resistance of BC cells to chemotherapy and metastasis of cancer cells

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Chen, Yu-Chih, Saswat Sahoo, Riley Brien, et al. "Single-cell RNA-sequencing of migratory breast cancer cells: discovering genes associated with cancer metastasis." Analyst 144, no. 24 (2019): 7296–309. http://dx.doi.org/10.1039/c9an01358j.

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We enriched migratory breast cancer cells with enhanced tumor formation and metastasis capability using microfluidics and performed single-cell RNA-sequencing to identify unique EMT and CSC signature of migratory cells.

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Bozgeyik, Esra. "MicroRNA-17-5p targets expression of cancer-associated genes in breast cancer cells." Meta Gene 24 (June 2020): 100614. http://dx.doi.org/10.1016/j.mgene.2019.100614.

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