ArticleCell proliferation2019
ERα is required for suppressing OCT4-induced proliferation of breast cancer cells via DNMT1/ISL1/ERK axis.
Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Review
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- High OCT4 Expression Might Be Associated with an Aggressive Phenotype in Rectal Cancer.Cancers · 2023Article
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- Marker-free characterization of full-length transcriptomes of single live circulating tumor cells.Genome research · 2023Article
- miR-142-5p Inhibits Cell Invasion and Migration by Targeting DNMT1 in Breast Cancer.Oncology research · 2022Article
- Differential Expression of Steroid Hormone Receptors and Ten Eleven Translocation Proteins in Endometrial Cancer Cells.Frontiers in oncology · 2022Article
- Association Between SNPs in the One-Carbon Metabolism Pathway and the Risk of Female Breast Cancer in a Chinese Population.Pharmacogenomics and personalized medicine · 2022Article
- Metabolic and Epigenetic Regulation by Estrogen in Adipocytes.Frontiers in endocrinology · 2022Review
- CLDN6 Suppresses c-MYC-Mediated Aerobic Glycolysis to Inhibit Proliferation by TAZ in Breast Cancer.International journal of molecular sciences · 2021Article
- Estrogen Regulates Endoplasmic Reticulum Stress-Mediated Apoptosis by ERK-p65 Pathway to Promote Endometrial Angiogenesis.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Roles of the Immune/Methylation/Autophagy Landscape on Single-Cell Genotypes and Stroke Risk in Breast Cancer Microenvironment.Oxidative medicine and cellular longevity · 2021Article
- The U2AF2 /circRNA ARF1/miR-342-3p/ISL2 feedback loop regulates angiogenesis in glioma stem cells.Journal of experimental & clinical cancer research : CR · 2020Article
- Estradiol-Induced Epigenetically Mediated Mechanisms and Regulation of Gene Expression.International journal of molecular sciences · 2020Review
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
Abstract
objectivePOU5F1 (OCT4) is implicated in cancer stem cell self-renewal. Currently, some studies have shown that OCT4 has a dual function in suppressing or promoting cancer progression. However, the precise molecular mechanism of OCT4 in breast cancer progression remains unclear. MATERIALS AND
methodsRT-PCR and Western blot were utilized to investigate OCT4 expression in breast cancer tissues and cells. Cell proliferation assays and mouse models were applied to determine the effects of OCT4 on breast cancer cell proliferation. DNMT1 inhibitors, ChIP, CoIP, IHC and ERα inhibitors were used to explore the molecular mechanism of OCT4 in breast cancer.
resultsOCT4 was down-regulated in breast cancer tissues, and the overexpression of OCT4 promoted MDA-MB-231 cell proliferation and inhibited the proliferation of MCF-7 cells in vitro and in vivo, respectively. Two DNMT1 inhibitors (5-aza-dC and zebularine) suppressed OCT4-induced MDA-MB-231 cell proliferation through Ras/Raf1/ERK inactivation by targeting ISL1, which is the downstream of DNMT1. In contrast, OCT4 interacted with ERα, decreased DNMT1 expression and inactivated the Ras/Raf1/ERK signalling pathway in MCF-7 cells. Moreover, ERα inhibitor (AZD9496) reversed the suppression of OCT4-induced proliferation in MCF-7 cells via the activation of ERK signalling pathway.
conclusionsOCT4 is dependent on ERα to suppress the proliferation of breast cancer cells through DNMT1/ISL1/ERK axis.
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