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Journal articles on the topic 'Proto-Oncogene Proteins Cell Cycle Flow Cytometry'

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Published: 4 June 2021

Last updated: 5 February 2022

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1

Borwankar, Anagha, Alessandro Pastore, Aniruddha Deshpande, et al. "Regulation of the Cyclin D1 Proto-Oncogene by Cell Cycle Regulatory MicroRNAs." Blood 112, no. 11 (2008): 1801. http://dx.doi.org/10.1182/blood.v112.11.1801.1801.

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Abstract Mutations, activation or overexpression of cyclin D1 are common features of several human cancers including mantle cell lymphoma (MCL) which bears the characteristic t(11;14) translocation juxtaposing the cyclin D1 gene downstream of the immunoglobulin heavy chain enhancer. The loss of the 3’UTR of this gene has been reported in a majority of MCL patients as well as in cell lines. In order to assess the impact of the 3’UTR on cyclin D1 expression levels, we used YFP tagged cyclin D1 reporter plasmids to quantify cyclin D1 expression in cell lines with different mutations of the 3’UTR.

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Liang, Xiaolong, Yi Liu, Liqiong Zeng, et al. "ATL." International Journal of Gynecologic Cancer 24, no. 7 (2014): 1165–72. http://dx.doi.org/10.1097/igc.0000000000000187.

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ObjectivesThe chief objective of this study was to identify the miRNAs targeting Fos, a well-recognized proto-oncogene that is commonly overexpressed in cervical cancer, and its biological significance on the cellular behaviors of HeLa, a cervical cancer cell.Materials and MethodsWe initially analyzed the 3′untranslated region (3′UTR) of Fos and screened the potential miRNAs targeting Fos using 3 bioinformatical Web sites. Luciferase reporter assay, real-time polymerase chain reaction, and Western blotting were used to validate the binding of chosen miRNA (miR-101) on the 3′UTR of Fos and the

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Wang, Jianwei, Jinhui Zhu, Mingjun Dong, Hua Yu, Xiaoyu Dai, and Keqiang Li. "Knockdown of Tripartite Motif Containing 24 by Lentivirus Suppresses Cell Growth and Induces Apoptosis in Human Colorectal Cancer Cells." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 22, no. 1 (2014): 39–45. http://dx.doi.org/10.3727/096504014x14078436005012.

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Colorectal cancer remains one of the most common cancers in men and women, and it accounts for a large proportion of cancer-related deaths worldwide. Tripartite motif (TRIM) proteins are a novel class of single protein RING finger E3 ubiquitin ligases, which have been shown to be involved in many cancers. The aim of this study was to investigate the potential role of TRIM24 in human colorectal cancer. By using a lentivirus-mediated RNA interference system, we first explored the effect of TRIM24 knockdown on HCT116 cell proliferation and colony formation. Moreover, flow cytometry analysis was u

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Zhao, Zhen, Yan Xing, Fei Yang, et al. "LncRNA HOXA-AS2 Promotes Oral Squamous Cell Proliferation, Migration, and Invasion via Upregulating EZH2 as an Oncogene." Technology in Cancer Research & Treatment 20 (January 2021): 153303382110391. http://dx.doi.org/10.1177/15330338211039109.

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Oral squamous cell carcinoma (OSCC) is one of the most common types of cancer worldwide. Accumulating evidence has shown that long noncoding RNAs (lncRNAs) serve important roles in the development of OSCC. The purpose of this study was to investigate the biological function and underlying regulatory mechanism of lncRNA homeobox A cluster antisense RNA2 (HOXA-AS2) in OSCC. RT-qPCR was performed to analyze the HOXA-AS2 expressions in human immortalized oral epithelial cell (HIOEC) line, human OSCC cell lines, and plasma. The expression of HOXA-AS2 and enhancer of zeste 2 polycomb repressive comp

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Blanton, Wanda P., Fangnian Wang, Hongsheng Liu, Paul Romesser, Douglas Faller, and Gerald Denis. "The Dual Bromodomain Protein Brd2 Controls Primary B Cell Mitogenesis and Cell Cycle in Mice Reconstituted with Lentivirus-Transduced HSCs." Blood 112, no. 11 (2008): 2465. http://dx.doi.org/10.1182/blood.v112.11.2465.2465.

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Abstract Transcriptional control of cellular proliferation and differentiation is critically important in hematopoiesis; specifically, the role of chromatin-dependent regulatory processes in this context is poorly understood. The human BRD2 proto-oncogene encodes a double bromodomain protein that binds to acetylated histone H4 in chromatin and is located within the MHC class II locus, suggesting Brd2 plays a role in immunity. However, BRD2 shares no sequence similarity with other MHC genes, nor is Brd2 involved in antigen processing, but rather it plays a role in mitogenic signal transduction.

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Liu, Kuiran, Tianda Feng, Jie Liu, Ming Zhong та Shulan Zhang. "Silencing of the DEK gene induces apoptosis and senescence in CaSki cervical carcinoma cells via the up-regulation of NF-κB p65". Bioscience Reports 32, № 3 (2012): 323–32. http://dx.doi.org/10.1042/bsr20100141.

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The human DEK proto-oncogene has been found to play an important role in autoimmune disease, viral infection and human carcinogenesis. Although it is transcriptionally up-regulated in cervical cancer, its intracellular function and regulation is still unexplored. In the present study, DEK and IκBα [inhibitor of NF-κB (nuclear factor κB) α] shRNAs (short hairpin RNAs) were constructed and transfected into CaSki cells using Lipofectamine™. The stable cell line CaSki–DEK was obtained after G418 selection. CaSki–IκB cells were observed at 48 h after psiRNA-IκB transfection. The inhibitory efficien

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Kallal, Lorena A., Anna Waszkiewicz, Jon-Paul Jaworski, et al. "High-Throughput Screening and Triage Assays Identify Small Molecules Targeting c-MYC in Cancer Cells." SLAS DISCOVERY: Advancing the Science of Drug Discovery 26, no. 2 (2021): 216–29. http://dx.doi.org/10.1177/2472555220985457.

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While c-MYC is well established as a proto-oncogene, its structure and function as a transcription factor have made c-MYC a difficult therapeutic target. To identify small-molecule inhibitors targeting c-MYC for anticancer therapy, we designed a high-throughput screening (HTS) strategy utilizing cellular assays. The novel approach for the HTS was based on the detection of cellular c-MYC protein, with active molecules defined as those that specifically decreased c-MYC protein levels in cancer cells. The assay was based on a dual antibody detection system using Förster/fluorescence resonance ene

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Zhou, Riyong, Ruye Ma, Zhenlin Jin, Liyuan Tang, Ying Zhou, and Yu Zhang. "Resveratrol increases the sensitivity of multiple myeloma cells against bortezomib via Hedgehog signaling pathway." Tropical Journal of Pharmaceutical Research 18, no. 10 (2021): 2133–38. http://dx.doi.org/10.4314/tjpr.v18i10.19.

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Purpose: To investigate the effect of resveratrol (RSV) on bortezomib (BTZ)-resistant multiple myeloma (MM) cells, and to elucidate the underlying mechanism of action. Methods: H929 cell lines were exposed to BTZ for 8 months to establish BTZ-resistant MM cell model. Cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was measured using annexin V/propidium iodide (PI) staining while cell cycle analysis was evaluated by flow cytometry. The expression of Hedgehog (Hh) signaling proteins (sonic hedgehog (SHH), smoothened (

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McDonnell, T. J., G. Nunez, F. M. Platt, et al. "Deregulated Bcl-2-immunoglobulin transgene expands a resting but responsive immunoglobulin M and D-expressing B-cell population." Molecular and Cellular Biology 10, no. 5 (1990): 1901–7. http://dx.doi.org/10.1128/mcb.10.5.1901.

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We characterized the basis for the follicular lymphoproliferation in transgenic mice bearing a Bcl-2-immunoglobulin (Bcl-2-Ig) minigene representing the t(14;18) of human follicular lymphoma. Discriminatory S1 nuclease protection assays revealed that the Bcl-2-Ig transgene was overexpressed relative to endogenous mouse Bcl-2 in spleen and thymus. Western (immunoblot) analysis demonstrated the overproduction of the human 25-kilodalton Bcl-2 protein, which arose from the transgene, in spleen, thymus, and the expanded B-cell subset. Despite the generalized lymphoid pattern of deregulation, two-co

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McDonnell, T. J., G. Nunez, F. M. Platt, et al. "Deregulated Bcl-2-immunoglobulin transgene expands a resting but responsive immunoglobulin M and D-expressing B-cell population." Molecular and Cellular Biology 10, no. 5 (1990): 1901–7. http://dx.doi.org/10.1128/mcb.10.5.1901-1907.1990.

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We characterized the basis for the follicular lymphoproliferation in transgenic mice bearing a Bcl-2-immunoglobulin (Bcl-2-Ig) minigene representing the t(14;18) of human follicular lymphoma. Discriminatory S1 nuclease protection assays revealed that the Bcl-2-Ig transgene was overexpressed relative to endogenous mouse Bcl-2 in spleen and thymus. Western (immunoblot) analysis demonstrated the overproduction of the human 25-kilodalton Bcl-2 protein, which arose from the transgene, in spleen, thymus, and the expanded B-cell subset. Despite the generalized lymphoid pattern of deregulation, two-co

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WILSON, Nicholas J., Suzanne T. MOSS, Xavier F. CSAR, Alister C. WARD, and John A. HAMILTON. "Protein phosphatase 2A is expressed in response to colony-stimulating factor 1 in macrophages and is required for cell cycle progression independently of extracellular signal-regulated protein kinase activity." Biochemical Journal 339, no. 3 (1999): 517–24. http://dx.doi.org/10.1042/bj3390517.

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Colony-stimulating factor 1 (CSF-1) is required for the development of monocytes/macrophages from progenitor cells and for the survival and activation of mature macrophages. The receptor for CSF-1 is the product of the c-fms proto-oncogene, which, on binding ligand, can stimulate a mitogenic response in the appropriate cells. To investigate which genes are regulated in response to CSF-1-stimulation in murine bone-marrow-derived macrophages (BMM), we employed mRNA differential display reverse transcriptase-mediated PCR to identify cDNA species induced by CSF-1. Both Northern and Western blot an

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Zhao, Nan, Shaheen Ahmed, Fei Wang, DiMaio J. Dominick, Chi Lin, and Chi Zhang. "Targeting the androgen receptor as a novel therapeutic strategy for high-grade gliomas by suppressing glioma cancer stem cells." Journal of Clinical Oncology 37, no. 15_suppl (2019): e13504-e13504. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e13504.

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e13504 Background: Glioblastoma (GBM) is the most aggressive and most common type of primary brain malignancies with median overall survival being only 20.9 months. The incidence of GBM is 50% greater in men than in women, and GBM transplanted into animals grow at a slower rate in females compared with males. Gender difference in GBM indicates that sex hormones such as androgen receptor (AR) may be involved in the tumorigenesis of GBM. A newer generation of AR antagonist, Enzalutamide, is available for prostate cancer treatment in clinic and can pass the blood-brain barrier, thus a good candid

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Chen, Weina, Ioannis Grammatikakis, Jiang Li, Vassiliki Leventaki, L. Jeffrey Medeiros, and George Z. Rassidakis. "Inhibition of AKT/mTOR Signaling Pathway Induces Cell Cycle Arrest and Apoptosis in Acute Myelogenous Leukemia." Blood 106, no. 11 (2005): 2355. http://dx.doi.org/10.1182/blood.v106.11.2355.2355.

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Abstract Acute myelogeneous leukemia (AML) is a heterogeneous disease and includes a subset of neoplasms that harbor activating mutations of the fms-like tyrosine kinase-3 (FLT3) gene. Mutated FLT3 has recently been shown to activate downstream oncogenic pathways including the PI3K/AKT pathway (Scheijen, et al. Oncogene. 23:3338–3349, 2004; Choudhary, et al. Blood. 106:265–273, 2005). It is known that activated AKT mediates its effects, at least in part, through activation of mammalian target of rapamycin (mTOR). However, the potential role of PI3K/AKT/mTOR signaling pathway in tumor cell surv

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Qiu, Shaowei, Jing Yu, Tengteng Yu, et al. "Sertad1 Antagonizes iASPP Function By Hindering Its Entrance into Nuclei to Interact with P53 in Leukemic Cells." Blood 124, no. 21 (2014): 5201. http://dx.doi.org/10.1182/blood.v124.21.5201.5201.

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Abstract Introduction: As the important suprressor of P53, iASPP was found to be overexpressed in leukemia, and functioned as oncogene that inhibited apoptosis of leukemia cells. Sertad1 is identified as one of the proteins that can bind with iASPP in our previous study by two-hybrid screen. Sertad1 is highly expressed in carcinomas from pancreatic, lung and ovarian tissues, which considered Sertad1 as an oncoprotein. In this study, our findings revealed that Sertad1 could interact with iASPP in the cytoplasm near nuclear membrane, which could block iASPP to enter into nucleus to interact with

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15

Xie, Yi ngqiu, Mehmet Burcu, and Maria R. Baer. "PKC412 Directly Inhibits the Serine/Threonine Protein Kinase Pim-1 in Cell Lines and Acute Myeloid Leukemia Cells as a Novel Mechanism of Inhibition of Multidrug Resistance." Blood 112, no. 11 (2008): 2655. http://dx.doi.org/10.1182/blood.v112.11.2655.2655.

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Abstract The serine/threonine protein kinase Pim-1, encoded by a proto-oncogene originally identified as the proviral insertion site in Moloney murine leukemia virus lymphomagenesis, is frequently overexpressed in acute myeloid leukemia (AML) and other malignancies and has been implicated in regulation of both cell cycle and apoptosis. We recently demonstrated that Pim-1 also regulates drug resistance. Pim-1 phosphorylates and activates the ATP-binding cassette (ABC) transporters P-glycoprotein (Pgp; MDR1; ABCB1) and breast cancer resistance protein (BCRP; ABCG2), which are strongly associated

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Natarajan, Karthika, Mehmet Burcu, and Maria R. Baer. "Inhibition of the Serine/Threonine Kinase Pim-1 Has Anti-Proliferative Effects In Acute Myeloid Leukemia (AML) and Sensitizes Multidrug Resistant Cells to Chemotherapy." Blood 116, no. 21 (2010): 1832. http://dx.doi.org/10.1182/blood.v116.21.1832.1832.

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Abstract Abstract 1832 Poster Board I-812 The serine/threonine kinase Pim-1, encoded by a proto-oncogene originally identified as the proviral integration site in Moloney murine leukemia virus lymphomagenesis, phosphorylates and thereby increases expression of multiple cellular proteins, including the pro-apoptotic protein BAD, the cell cycle regulatory proteins p21, p27, Cdc25A and Cdc25C, the transcription factors SOCS-1, RUNX3 and c-myc and, as we recently demonstrated, the drug resistance-associated ATP-binding cassette (ABC) proteins P-glycoprotein (Pgp, ABCB1) and breast cancer resistanc

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Sachs, Zohar, Hanh Nguyen, Nurul Azyan Mohd Hassan, et al. "Activated NRAS Mediates Self-Renewal Capacity in AML by Facilitating the Mll/AF9-Specified Gene Expression Signature." Blood 120, no. 21 (2012): 5116. http://dx.doi.org/10.1182/blood.v120.21.5116.5116.

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Abstract Abstract 5116 RAS is a known oncogene in AML (Schubbert et al. Nat Rev Cancer 2007, Bowen et al. Blood 2006), however the specific effects of targeting RAS-activated pathways on AML physiology are unclear. NRASG12V transgene repression in an NRASG12V/Mll/AF9 transgenic murine AML model leads to apoptosis and disease remission (Kim et al. Blood 2009). To better understand possibilities for and implications of therapeutic targeting of RAS-activated pathways, we inactivate NRASG12V in this mouse model and characterize the subsequent signaling and transcriptional response. We profiled sig

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Soper, David M., Ying-Wen Huang, Francois Wilhelm, et al. "Single Cell Network Profiling (SCNP) to Evaluate the Mechanism of Action of ON 01910.Na, A Novel Clinical Trial Stage Compound." Blood 114, no. 22 (2009): 3827. http://dx.doi.org/10.1182/blood.v114.22.3827.3827.

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Abstract Abstract 3827 Poster Board III-763 Background ON 01910.Na, a small molecule multikinase inhibitor, promotes G2/M arrest and apoptosis. Key targets for this inhibitor include Plk1 (polo-like kinase, a cell cycle regulator), Cdk1, (cyclin dependent kinase, a mitotic regulator) and the PI-3 kinase pathway (Ramana Reddy et al. J. Med. Chem. 2008, Park et al, Oncogene, 2007, Gumireddy et al., Cancer Cell, 2005). The drug has been shown to have anti-tumor activity in in vitro and in vivo models. Phase I studies in >100 advanced cancer patients revealed that the drug is well tolerated. Fu

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Piya, Sujan, Hong Mu, Seemana Bhattacharya, et al. "BRD4 Proteolysis Targeting Chimera (PROTAC) ARV-825 Targets Both NOTCH1-MYC Regulatory Circuit and Leukemia-Microenvironment in T-ALL." Blood 130, Suppl_1 (2017): 716. http://dx.doi.org/10.1182/blood.v130.suppl_1.716.716.

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Abstract Background: Salvage options for patients with relapsed T cell acute lymphoblastic leukemia (T-ALL) are limited, with less than 25% of these patients achieving second remission 1, 2. 70% of T-ALL cases have activating mutations of the NOTCH1 pathway, which transcriptionally activates MYC by binding to its `superenhancer' region 3, 4. Other deregulated oncogenic pathways in T-ALL include PI3K/Akt, the anti-apoptotic Bcl-2 family, and CDKN2A/2B cell cycle regulators 5, 6. The NOTCH1-MYC regulatory circuit is an attractive therapeutic target, but clinical development of gamma-secretase in

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Martin, Gaëlle H., Alexis Desrichard, Stephen S. Chung, et al. "CD97 Is a Critical Regulator of Acute Myeloid Leukemia Stem Cell Function." Blood 128, no. 22 (2016): 1077. http://dx.doi.org/10.1182/blood.v128.22.1077.1077.

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Abstract Despite recent advances in our understanding of the genetic origins of acute myeloid leukemia (AML), clinical outcomes remain poor. While standard induction chemotherapy induces remission in most patients, the majority of patients eventually relapses and dies from progressive disease. A number of cell surface proteins have been shown to be expressed at high levels on AML stem cells compared to normal HSCs including CD47, CD44, CD96, TIM3, CD123, CD25 and IL1RAP. Despite the attention these antigens have received, data supporting their roles as cell-intrinsic regulators of LSCs are mor

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Hu, Kaimin, Lizhen Liu, Binsheng Wang та ін. "Bone Marrow Mesenchymal Stromal Cells Protect Acute Lymphocytic Leukemia Cells From Cytotoxic Agents Via MAPK/Erk and Wnt/β-Catenin Signal Pathways". Blood 120, № 21 (2012): 4736. http://dx.doi.org/10.1182/blood.v120.21.4736.4736.

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Abstract Abstract 4736 Acute lymphoblastic leukemia (ALL) remains one of the greatest challenges in oncology. Relapsed ALL is a leading cause of death in young people, and further improvements in outcome will required the development of therapeutic approaches directed against rational therapeutic targets. Increasing evidence indicated that the bone marrow microenvironment plays a crucial role in the pathogenesis of leukemia by promoting tumor cell growth and survival as well as drug resistance. As a pivotal component of the bone marrow microenvironment, how bone marrow derived mesenchymal stro

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Riveiro, Maria Eugenia, Lucile Astorgues-Xerri, Charlotte Canet-jourdan, et al. "Preclinical Evaluation of the BET-Bromodomain (BET-BRD) Inhibitor OTX015 in Leukemia Cell Lines Harboring the JAK2 V617F Mutation." Blood 124, no. 21 (2014): 873. http://dx.doi.org/10.1182/blood.v124.21.873.873.

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Abstract Background: Exposure of cancer cells to BET-BRD protein inhibitors has been associated with a significant downregulation of C-MYC expression, leading to suppression of the transcriptional program linked to proliferation and survival. C-MYC mRNA expression, mediated by STAT5 activation, is induced by the JAK2 (V617F) mutation (JAK2mu) in transfected BA/F3 cells (Funakoshi-Tago, et al. 2013). We selected JAK2mu leukemia-derived cell lines for preclinical evaluation of OTX015 (Oncoethix, Switzerland), a selective orally-bioavailable inhibitor of BET-BRD proteins with promising early resu

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Delia, D., A. Aiello, D. Soligo, et al. "bcl-2 proto-oncogene expression in normal and neoplastic human myeloid cells." Blood 79, no. 5 (1992): 1291–98. http://dx.doi.org/10.1182/blood.v79.5.1291.1291.

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Abstract The present study provides immunobiochemical and molecular data on the differentiation-linked expression of the bcl-2 proto-oncogene in normal and neoplastic myeloid cells. Using a recently developed monoclonal antibody (MoAb) to the bcl-2 molecule, staining of normal bone marrow myeloblasts, promyelocytes, and myelocytes, but neither monocytes nor most polymorphonuclear cells, was demonstrated. By two-color flow cytometric analysis, bcl-2 was evidenced in CD33+ and CD33+/CD34+ myeloid cells as well as in the more primitive CD33-/CD34+ population. The leukemic cell lines HL-60, KG1, G

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Delia, D., A. Aiello, D. Soligo, et al. "bcl-2 proto-oncogene expression in normal and neoplastic human myeloid cells." Blood 79, no. 5 (1992): 1291–98. http://dx.doi.org/10.1182/blood.v79.5.1291.bloodjournal7951291.

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The present study provides immunobiochemical and molecular data on the differentiation-linked expression of the bcl-2 proto-oncogene in normal and neoplastic myeloid cells. Using a recently developed monoclonal antibody (MoAb) to the bcl-2 molecule, staining of normal bone marrow myeloblasts, promyelocytes, and myelocytes, but neither monocytes nor most polymorphonuclear cells, was demonstrated. By two-color flow cytometric analysis, bcl-2 was evidenced in CD33+ and CD33+/CD34+ myeloid cells as well as in the more primitive CD33-/CD34+ population. The leukemic cell lines HL-60, KG1, GM-1, and

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Zhao, Huiwu, Anna Kalota, Shenghao Jin, and Alan Gewirtz. "The c-myb Protooncogene and microRNA (miR)-15a Form an Autoregulatory Loop That May Play a Role in Normal Human Erythropoiesis." Blood 110, no. 11 (2007): 2642. http://dx.doi.org/10.1182/blood.v110.11.2642.2642.

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Abstract The c-myb proto-oncogene encodes an obligate hematopoietic cell transcription factor that contributes to lineage commitment, proliferation, and differentiation. Factors which regulate c-myb expression are of interest but remain incompletely defined. MicroRNAs (miRNAs) are being increasingly recognized as important regulators of cell development, and abnormalities in miRNA activity may also contribute to the pathogenesis of several hematologic malignancies. We speculated that miRNAs might also regulate c-Myb expression, a gene often aberrantly expressed in leukemia, lymphoma, and myelo

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Masih-Khan, Esther, Suzanne Trudel, ZhiHua Li, et al. "Macrophage Inflammatory Protein (MIP)-1alpha (CCL3) Is a Downstream Target of FGFR3 and RAS Signaling in Multiple Myeloma." Blood 106, no. 11 (2005): 251. http://dx.doi.org/10.1182/blood.v106.11.251.251.

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Abstract The identification of the t(4;14) translocation in Multiple Myeloma (MM) provided the first indication that fibroblast growth factor 3 (FGFR3) could act as an oncogene. Several studies have assessed the potential of FGFR3 as a drug target and have shown that inhibition of FGFRs using tyrosine kinase inhibitors induces cell death of FGFR3 expressing MM cells. To clarify the signaling pathways implicated in FGFR3 dependent myeloma, we assessed gene expression changes associated with treatment of MM cell lines with three known small molecule FGFR inhibitors, PD173074, SU5402 and a third

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Andreeff, M., DE Slater, J. Bressler, and ME Furth. "Cellular ras oncogene expression and cell cycle measured by flow cytometry in hematopoietic cell lines." Blood 67, no. 3 (1986): 676–81. http://dx.doi.org/10.1182/blood.v67.3.676.bloodjournal673676.

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Human hematopoietic malignancies provide an excellent model for the study of the activity of cellular oncogenes in a context of known defects in cell proliferation and differentiation. A flow cytometric immunofluorescence assay was developed to quantitate the expression of the cellular ras oncogenes in relation to the cell cycle in individual leukemic cells. Specific binding of a monoclonal antibody to the 21-kd protein (p21ras) encoded by the Ha-ras, Ki-ras, and N-ras genes was measured by flow cytometry and confirmed by fluorescence microscopy. P21ras was detected in 416B, a murine hematopoi

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Senapedis, William, Ryan George, Dilara McCauley, et al. "Novel Selective Orally Bioavailable Small Molecule PAK4 Allosteric Modulators (PAMs) Display Anti-Tumor Activity in Vitro and in Vivo in Hematological Malignancies." Blood 124, no. 21 (2014): 2208. http://dx.doi.org/10.1182/blood.v124.21.2208.2208.

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Abstract Introduction: Many hematological cancers have been successfully treated through identification of specialized targets in each specific tumor subtype (e.g. BTK inhibition in NHL or proteasome inhibition in multiple myeloma). The p21-Activated Kinase 4 (PAK4) is critical to cellular signaling and may represent a new target for therapy in many hematologic malignancies. PAK4 is a member of the PAK family of proteins that regulate cell survival, cell division and apoptosis. The six members of the PAK family are divided into two groups; Group I (PAK1, 2, 3) and Group II (PAK4, 5, 6), based

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Andreeff, M., DE Slater, J. Bressler, and ME Furth. "Cellular ras oncogene expression and cell cycle measured by flow cytometry in hematopoietic cell lines." Blood 67, no. 3 (1986): 676–81. http://dx.doi.org/10.1182/blood.v67.3.676.676.

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Abstract Human hematopoietic malignancies provide an excellent model for the study of the activity of cellular oncogenes in a context of known defects in cell proliferation and differentiation. A flow cytometric immunofluorescence assay was developed to quantitate the expression of the cellular ras oncogenes in relation to the cell cycle in individual leukemic cells. Specific binding of a monoclonal antibody to the 21-kd protein (p21ras) encoded by the Ha-ras, Ki-ras, and N-ras genes was measured by flow cytometry and confirmed by fluorescence microscopy. P21ras was detected in 416B, a murine

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Seca, Hugo, Raquel T. Lima, Vanessa Lopes-Rodrigues, Jose E. Guimaraes, Gabriela M. Almeida, and M. Helena Vasconcelos. "Antimir-21 Causes Autophagy in the K562 Cell Line and Sensitizes Cells to the Effect of Doxorubicin and Etoposide." Blood 120, no. 21 (2012): 4908. http://dx.doi.org/10.1182/blood.v120.21.4908.4908.

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Abstract Abstract 4908 Background: microRNAs (miRs) are short non-coding RNAs that regulate gene expression by binding to targeted mRNAs and causing their degradation or inhibition of translation. Some miRs have been described to play a role in disease pathogenesis and response to therapy in cancer [Lee and Dutta (2009), Annu Rev Pathol 4:199–227]. Other miRs have been associated with cancer drug resistance. For example, miR-21 has been shown to be involved in chemoresistance in a variety of cancer cells, namely leukemia cells [Li et al. (2010), Hematology 15:215–21] and to target several gene

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Pasquier, Florence, Carole Tonetti, Rodolphe Besancenot, et al. "Interferon-Alpha Preferentially Targets JAK2V617F-Positive Rather Than Wild-Type Early Progenitor Cells in Myeloproliferative Disorders." Blood 114, no. 22 (2009): 436. http://dx.doi.org/10.1182/blood.v114.22.436.436.

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Abstract Abstract 436 Polycythemia vera (PV), essential thrombocytemia (ET) and primary myelofibrosis (PMF) are myeloproliferative disorders (MPDs) without curative treatment, unless hematopoietic stem cell (HSC) transplantation is performed. However, for several years the use of interferon-alpha (IFNα) has provided an efficient therapeutic alternative for MPD patients. IFNα was shown to induce complete long-term hematologic and molecular remissions in JAK2V617F-positive MPD patients, suggesting a possible curative effect of IFNα. In order to better understand mechanisms of action of this drug

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Reidy, Mairead, Marianne VanDijk, Michael O'Neill, and Michael O'Dwyer. "The Dual PIM/PI3-K Inhibitor Ibl-202 Overcomes Microenvironmental Mediated Resistance in Multiple Myeloma and Prevents PIM1 Induced CXCR4 Upregulation." Blood 126, no. 23 (2015): 5350. http://dx.doi.org/10.1182/blood.v126.23.5350.5350.

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Abstract Background: The interaction of multiple myeloma (MM) cells with bone marrow (BM) cells along with factors in the BM milieu such as chemokines and cytokines play a crucial role in both progression of MM and drug resistance. Activation of the PI3-K/Akt survival pathway is a characteristic of both human MM cell lines and patient samples. This activation can be linked to BM microenvironmental signalling and use of proteasome inhibitors in treatment, suggesting this as a crucial point of therapeutic intervention to abrogate growth and survival signals in MM. However, the efficacy of such t

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Kawamoto, K., T. Okada, Y. Kannan, H. Ushio, M. Matsumoto, and H. Matsuda. "Nerve growth factor prevents apoptosis of rat peritoneal mast cells through the trk proto-oncogene receptor." Blood 86, no. 12 (1995): 4638–44. http://dx.doi.org/10.1182/blood.v86.12.4638.bloodjournal86124638.

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We investigated the inhibitory activity of nerve growth factor (NGF) on apoptosis of rat peritoneal mast cells (PMCs) and compared it with that of recombinant stem cell factor (rSCF), which is a mast cell growth factor. When PMCs were incubated up to 72 hours in the presence of control medium, internucleosomal fragmentation of DNA indicating apoptosis was detected by agarose gel electrophoresis and flow cytometry. The aged PMCs showed morphological changes typical for apoptosis, such as chromatin condensation and loss of microvilli of the cell membrane. Addition of NGF or rSCF prevented develo

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Li, Cuilan, Vincent Wing Sun Liu, David Wai Chan, Kwok Ming Yao, and Hextan Yuen Sheung Ngan. "LY294002 and Metformin Cooperatively Enhance the Inhibition of Growth and the Induction of Apoptosis of Ovarian Cancer Cells." International Journal of Gynecologic Cancer 22, no. 1 (2012): 15–22. http://dx.doi.org/10.1097/igc.0b013e3182322834.

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BackgroundThe phosphoinositide 3 kinase (PI3K)/v-akt murine thymoma viral oncogene homolog (AKT)/mammalian target of rapamycin (mTOR) pathway is frequently aberrantly activated in ovarian cancer and confers the chemoresistant phenotype of ovarian cancer cells. LY294002 (PI3K inhibitor) and metformin (5′-adenosine monophosphate [AMP]-activated protein kinase [AMPK] activator) are 2 drugs that were known to inhibit mTOR expression through the AKT-dependent and AKT-independent pathways, respectively. In this study, we explored the effectiveness of LY294002 and metformin in combination on inhibiti

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Chen, Jingfei, Yun Shi, Jingrui Huang, Jiefeng Luo, and Weishe Zhang. "Neuromedin B receptor mediates neuromedin B-induced COX-2 and IL-6 expression in human primary myometrial cells." Journal of Investigative Medicine 68, no. 6 (2020): 1171–78. http://dx.doi.org/10.1136/jim-2020-001412.

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The precise mechanisms that lead to parturition remain unclear. In our initial complementary DNA (cDNA) microarray experiment, we found that the neuromedin B receptor (NMBR) was differentially expressed in the human myometrium during spontaneous or oxytocin-induced labor. We have previously shown that neuromedin B (NMB) could induce interleukin 6 (IL-6) and type 2 cyclo-oxygenase enzyme (COX-2) expression in the primary human myometrial cells via nuclear factor kappa B (NF-κB) transcription factor p65 (p65) and Jun proto-oncogene, activator protein 1 (AP-1) transcription factor subunit (c-Jun)

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Baran, Natalia, Alessia Lodi, Yogesh Dhungana, et al. "Overcoming NOTCH1-Driven Chemoresistance in T-Cell Acute Lymphoblastic Leukemia Via Metabolic Intervention with Oxphos Inhibitor." Blood 136, Supplement 1 (2020): 18–20. http://dx.doi.org/10.1182/blood-2020-136801.

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The inferior cure rate of T-cell acute lymphoblastic leukemia (T-ALL) is associated with inherent drug resistance. The activating NOTCH1 gene mutations have been reported to cause chemoresistance at the stem cell level1. Direct NOTCH1 inhibition has failed in clinical trials due to a narrow therapeutic window but targeting key oncogenic and metabolic pathways downstream of mutated NOTCH1 may offer novel approaches. We previously reported that rapid transformation of thymocytes at the DN3 differentiation stage into preleukemic stem cells (pre-LSC) requires elevated Notch1 in addition to the pre

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Li, Zhi-feng, Wei-wei Xu, Ji-dan Li, Feng-ling Tao, Jian-xin Chen, and Jin-hua Xu. "Nucleotide exchange factor SIL1 promotes the progress of breast cancer cells via regulating the cell cycle and apoptosis." Science Progress 103, no. 1 (2019): 003685041989104. http://dx.doi.org/10.1177/0036850419891046.

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Breast cancer, as one of the most malignant tumors, poses a serious threat to the lives of females. Nucleotide exchange factor SIL1 is an important regulator of endoplasmic reticulum function that might have a specific role in tumor progression. In this study, we aimed to investigate the effect of SIL1 on the proliferation, apoptosis, and metastasis of human breast cancer. SIL1-specific small interfering RNA was transfected into two breast cancer cell lines, MCF7 and MDA-MB-231, to generate SIL1 knockdown cells. Clone formation and Cell Counting Kit-8 assays were performed to determine cell pr

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Lei, Xiangli, Meiling Yang, Zhifang Xiao, Heng Zhang, and Shuai Tan. "circTLK1 facilitates the proliferation and metastasis of renal cell carcinoma by regulating miR-495-3p/CBL axis." Open Life Sciences 16, no. 1 (2021): 362–74. http://dx.doi.org/10.1515/biol-2021-0041.

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Abstract Renal cell carcinoma (RCC) is a common urological malignancy. Circular RNAs (circRNAs) have been confirmed to play an important regulatory role in various cancers. This study aimed to investigate the role and potential mechanism of circTLK1 (hsa_circ_0004442) in RCC. The levels of circTLK1, Cbl proto-oncogene (CBL), and microRNA-495-3p (miR-495-3p) were detected by quantitative reverse transcription polymerase chain reaction or western blot. Cell proliferation, cycle arrest and apoptosis, migration, and invasion were assessed by colony formation, flow cytometry, scratch, and transwell

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Pan, Jie, Zongbin Xu, Meifang Xu, Xiaoyan Lin, Bingqiang Lin, and Mengxin Lin. "Knockdown of Forkhead box A1 suppresses the tumorigenesis and progression of human colon cancer cells through regulating the phosphatase and tensin homolog/Akt pathway." Journal of International Medical Research 48, no. 12 (2020): 030006052097145. http://dx.doi.org/10.1177/0300060520971453.

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Background This study aimed to evaluate the role and the underlying mechanisms of Forkhead box A1 (encoded by FOXA1) in colon cancer. Methods We analyzed FOXA1 mRNA and protein expression in colon cancer tissues and cell lines. We also silenced FOXA1 expression in HCT116 and SW480 cells to evaluate the effects on cell proliferation, cell cycle, migration, and invasion by using MTT, colony formation, flow cytometry, and the Transwell assay, respectively. Results FOXA1 immunostaining was higher in colon cancer tissues than adjacent healthy tissues. FOXA1 mRNA and protein expression was significa

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Zhao, Jiaojiao, Yuchen Pan, Xiujun Li, et al. "Dihydroartemisinin and Curcumin Synergistically Induce Apoptosis in SKOV3 Cells Via Upregulation of MiR-124 Targeting Midkine." Cellular Physiology and Biochemistry 43, no. 2 (2017): 589–601. http://dx.doi.org/10.1159/000480531.

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Background/Aim: Women with advanced ovarian carcinoma are less likely to receive platinum-based chemotherapy and surgery due to a greater risk of cytotoxicity and poorer outcomes. We attempted to improve a promising therapy against ovarian cancer by using a combination of dihydroartemisinin (DHA) and curcumin (Cur). Methods: Human ovarian cancer SKOV3 cells were treated with DHA, Cur alone, or a combination of both. The viability of SKOV3 cells was measured by Cell Counting Kit-8 (CCK-8) and a colony formation assay. The cell cycle and apoptosis of SKOV3 cells were monitored by flow cytometry.

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Meng, Fanling, Xiuwei Chen, Hongtao Song, and Ge Lou. "LAPTM4B Down Regulation Inhibits the Proliferation, Invasion and Angiogenesis of HeLa Cells In Vitro." Cellular Physiology and Biochemistry 37, no. 3 (2015): 890–900. http://dx.doi.org/10.1159/000430216.

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Background/Aims: LAPTM4B (lysosome-associated protein transmembrane 4 beta) is a novel oncogene with important functions in aggressive human carcinomas, including cervical cancer. However, the specific functions and internal molecular mechanisms associated with this gene in the context of cervical cancer remain unclear. Methods: In this study, we explored the effects and mechanisms of LAPTM4B on tumor growth, metastasis and angiogenesis in vitro by depletion of LAPTM4B in Hela cell. RNA interference was used to induce down regulation of LAPTM4B gene expression in Hela cells. The motility, migr

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Bona, Amanda Braga, Danielle Queiroz Calcagno, Helem Ferreira Ribeiro, et al. "Menadione reduces CDC25B expression and promotes tumor shrinkage in gastric cancer." Therapeutic Advances in Gastroenterology 13 (January 2020): 175628481989543. http://dx.doi.org/10.1177/1756284819895435.

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Background: Gastric cancer is one of the most incident types of cancer worldwide and presents high mortality rates and poor prognosis. MYC oncogene overexpression is a key event in gastric carcinogenesis and it is known that its protein positively regulates CDC25B expression which, in turn, plays an essential role in the cell division cycle progression. Menadione is a synthetic form of vitamin K that acts as a specific inhibitor of the CDC25 family of phosphatases. Methods: To better understand the menadione mechanism of action in gastric cancer, we evaluated its molecular and cellular effects

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Lerner, NB, KH Nocka, SR Cole, et al. "Monoclonal antibody YB5.B8 identifies the human c-kit protein product." Blood 77, no. 9 (1991): 1876–83. http://dx.doi.org/10.1182/blood.v77.9.1876.1876.

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Abstract The c-kit proto-oncogene encodes a 145- to 160-Kd transmembrane tyrosine kinase, which is a member of the platelet-derived growth factor receptor family and is allelic with the murine white spotting locus (W). W mutations affect several aspects of hematopoiesis, most notably erythroid progenitors and mast cells. A monoclonal antibody, YB5.B8, had been raised against the leukemic blasts of a patient with M1-type acute myelocytic leukemia (AML) and it precipitates a 150-Kd cell surface glycoprotein from leukemic cells. The YB5.B8 epitope is expressed on mast cells, on up to 3% of normal

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Lerner, NB, KH Nocka, SR Cole, et al. "Monoclonal antibody YB5.B8 identifies the human c-kit protein product." Blood 77, no. 9 (1991): 1876–83. http://dx.doi.org/10.1182/blood.v77.9.1876.bloodjournal7791876.

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The c-kit proto-oncogene encodes a 145- to 160-Kd transmembrane tyrosine kinase, which is a member of the platelet-derived growth factor receptor family and is allelic with the murine white spotting locus (W). W mutations affect several aspects of hematopoiesis, most notably erythroid progenitors and mast cells. A monoclonal antibody, YB5.B8, had been raised against the leukemic blasts of a patient with M1-type acute myelocytic leukemia (AML) and it precipitates a 150-Kd cell surface glycoprotein from leukemic cells. The YB5.B8 epitope is expressed on mast cells, on up to 3% of normal mononucl

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Mohammad, Hanan, Daniel j. Lindner, and Michael Kalafatis. "Casein Kinase CK2 Inhibition Results in Tumor Suppression." Blood 114, no. 22 (2009): 5052. http://dx.doi.org/10.1182/blood.v114.22.5052.5052.

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Abstract Abstract 5052 Protein Kinase II (CK2) is a pleiotropic, and ubiquitous serine/threonine kinase taht utilizes both ATP and GTP as phosphate donors. Protein kinase CK2 mostly exists as a tetramer composed of two catalytic subunits α and α‘, which exists in heterogeneous or homogenous nature, and two regulatory β subunits. CK2 is a key regulator of signaling pathways involved in cell cycle, proliferation and apoptosis. It is consistently overexpressed in cancer tissue and capable of shuttling between cellular compartments but mainly localized in the nuclear matrix of cancer cells. CK2 is

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Bjeije, Hassan, Bahram Mohammad Soltani, Mehrdad Behmanesh, and Mohammad Reza Zali. "YWHAE long non-coding RNA competes with miR-323a-3p and miR-532-5p through activating K-Ras/Erk1/2 and PI3K/Akt signaling pathways in HCT116 cells." Human Molecular Genetics 28, no. 19 (2019): 3219–31. http://dx.doi.org/10.1093/hmg/ddz146.

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AbstractYWHAE gene product belongs to the 14-3-3 protein family that mediates signal transduction in plants and mammals. Protein-coding and non-coding RNA (lncRNA) transcripts have been reported for this gene in human. Here, we aimed to functionally characterize YWHAE-encoded lncRNA in colorectal cancer-originated cells. RNA-seq analysis showed that YWHAE gene is upregulated in colorectal cancer specimens. Additionally, bioinformatics analysis suggested that YWHAE lncRNA sponges miR-323a-3p and miR-532-5p that were predicted to target K-Ras 3′UTR sequence. Overexpression of YWHAE lncRNA result

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Hu, Chao, Xiaobin Zhu, Taogen Zhang, et al. "Tanshinone IIA Inhibits Osteosarcoma Growth through a Src Kinase-Dependent Mechanism." Evidence-Based Complementary and Alternative Medicine 2021 (June 30, 2021): 1–15. http://dx.doi.org/10.1155/2021/5563691.

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Introduction. Osteosarcoma is a malignant tumor associated with high mortality rates due to the toxic side effects of current therapeutic methods. Tanshinone IIA can inhibit cell proliferation and promote apoptosis in vitro, but the exact mechanism is still unknown. The aims of this study are to explore the antiosteosarcoma effect of tanshinone IIA via Src kinase and demonstrate the mechanism of this effect. Materials and Methods. Osteosarcoma MG-63 and U2-OS cell lines were stable transfections with Src-shRNA. Then, the antiosteosarcoma effect of tanshinone IIA was tested in vitro. The protei

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Sheen, Joon-Ho, and Robert B. Dickson. "Overexpression of c-Myc Alters G1/S Arrest following Ionizing Radiation." Molecular and Cellular Biology 22, no. 6 (2002): 1819–33. http://dx.doi.org/10.1128/mcb.22.6.1819-1833.2002.

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ABSTRACT Study of the mechanism(s) of genomic instability induced by the c-myc proto-oncogene has the potential to shed new light on its well-known oncogenic activity. However, an underlying mechanism(s) for this phenotype is largely unknown. In the present study, we investigated the effects of c-Myc overexpression on the DNA damage-induced G1/S checkpoint, in order to obtain mechanistic insights into how deregulated c-Myc destabilizes the cellular genome. The DNA damage-induced checkpoints are among the primary safeguard mechanisms for genomic stability, and alterations of cell cycle checkpoi

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Link, Kevin A., Shan Lin, Kakajan Komurov, Mark Wunderlich, and James C. Mulloy. "Oncogene Dosage Is a Major Determinant of Leukemogenic Transformation by AE9a." Blood 118, no. 21 (2011): 1358. http://dx.doi.org/10.1182/blood.v118.21.1358.1358.

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Abstract Abstract 1358 Chromosomal translocation (8;21) results in the formation of the AML1-ETO (AE) leukemia-associated fusion protein. Roughly 70% of AE+ patient samples also harbor an alternatively spliced variant of AE, termed AE9a. AE9a promotes the leukemic transformation of mouse hematopoietic stem/progenitor cells without the need for secondary external cooperating oncogenes. By comparison, leukemia development in response to expression of full length AE requires one or more additional events. We extended these findings into a human cell system to determine whether AE9a is able to pro

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Ma, Jing, Xinrui Chen, Baoli Xu, and Wenguang Liu. "Quinolinone inhibits proliferation of gastric cancer cells and induces their apoptosis via down-regulation of the expression of pro-oncogene c-Myc." Tropical Journal of Pharmaceutical Research 19, no. 8 (2020): 1599–604. http://dx.doi.org/10.4314/tjpr.v19i8.5.

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Purpose: To determine the anti-proliferative potential of quinolinone against gastric cancer cells, and the underlying mechanism of action.Methods: Quinolinone-mediated proliferative changes were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, while its effect on apoptosis was determined by flow cytometry. Transwell and wound healing assays were used for the determination of the effect of quinolinone on cell invasion and migration. The effect of quinolinone on protein expression levels were assayed with western blotting.Results: Quinolinone caused redu

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