ArticleMolecular and cellular biochemistry2013
17β-estradiol up-regulates miR-155 expression and reduces TP53INP1 expression in MCF-7 breast cancer cells.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- Time-resolved RNA signatures of CD4+ T cells in Parkinson's disease.Cell death discovery · 2023Article
- miR-155-3p: processing by-product or rising star in immunity and cancer?Open biology · 2022Review
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- MicroRNA miR-155 is required for expansion of regulatory T cells to mediate robust pregnancy tolerance in mice.Mucosal immunology · 2020Article
- Relationship between miR-155 and miR-146a polymorphisms and susceptibility to multiple sclerosis in an Egyptian cohort.Biomedical reports · 2020Article
- NT21MP negatively regulates paclitaxel-resistant cells by targeting miR‑155‑3p and miR‑155-5p via the CXCR4 pathway in breast cancer.International journal of oncology · 2018Article
- The correlation of circulating pro-angiogenic miRNAs' expressions with disease risk, clinicopathological features, and survival profiles in gastric cancer.Cancer medicine · 2018Article
- Inferring potential small molecule-miRNA association based on triple layer heterogeneous network.Journal of cheminformatics · 2018Article
- Nanoparticle-Mediated Therapeutic Agent Delivery for Treating Metastatic Breast Cancer-Challenges and Opportunities.Nanomaterials (Basel, Switzerland) · 2018Review
- Estrogen-induced miR-196a elevation promotes tumor growth and metastasis via targeting SPRED1 in breast cancer.Molecular cancer · 2018Article
- Morin promotes prostate cancer cells chemosensitivity to paclitaxel through miR-155/GATA3 axis.Oncotarget · 2017Article
- Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features.International journal of oncology · 2017Article
- MicroRNA-155 promotes apoptosis in SKOV3, A2780, and primary cultured ovarian cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Soy Isoflavone Genistein-Mediated Downregulation of miR-155 Contributes to the Anticancer Effects of Genistein.Nutrition and cancer · 2016Article
- miRNAs regulated by estrogens, tamoxifen, and endocrine disruptors and their downstream gene targets.Molecular and cellular endocrinology · 2015Review
- Article
- Role of MK2 signaling pathway in the chronic compression of cervical spinal cord.American journal of translational research · 2015Article
- microRNA regulation of mammalian target of rapamycin expression and activity controls estrogen receptor function and RAD001 sensitivity.Molecular cancer · 2014Article
- miR-155 induced transcriptome changes in the MCF-7 breast cancer cell line leads to enhanced mitogen activated protein kinase signaling.Genes & cancer · 2014Article
- MicroRNAs in lupus.Autoimmunity · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In estrogen responsive breast cancer cells, estradiol (E2) is a key regulator of cell proliferation and survival. MiR-155 has emerged as an "oncomiR", which is the most significantly up-regulated miRNA in breast cancer. Moreover, miR-155 is higher in ERα (+) breast tumors than ERα (-), but no one has examined whether E2 regulates miR-155 expression in MCF-7 cells. In this study, the aim was to explore whether miR-155 involved in E2 regulated expression of estrogen responsive genes. We evaluated miR-155 expression in human breast cancer cells by real-time PCR, finding out miR-155 was overexpressed in MCF-7 cells compared with MDA-MB-231 cells. Treatment with E2 in MCF-7 cells increased miR-155 expression, promoting proliferation and decreasing apoptosis, similarly, transfection of miR-155m to MCF-7 cells gave the similar results. In contrast, inhibited miR-155 expression by transfection with miR-155 inhibitors reduced proliferation and promoted apoptosis of MCF-7 cells. Moreover, TP53INP1 is one of the targets of miR-155. E2 negatively regulated TP53INP1 mRNA expression and the protein expression of TP53INP1, cleaved-caspase-3, -8, -9, and p21, whereas transfection with miR-155 inhibitors increased TP53INP1, cleaved-caspase-3, -8, -9, and p21 protein level. These results demonstrated that E2 promoted breast cancer development and progression possibly through increasing the expression of miR-155, which was overexpressed in MCF-7 cells, contributes to proliferation of MCF-7 cells possibly through down-regulating TP53INP1.
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