MicroRNA-10b regulates proliferation, cell cycle and apoptosis in human breast cancer cells

GU Yi; LI Xiaoman; ZHENG Lufeng; YANG Jue; XI Tao

doi:10.11665/j.issn.1000-5048.20150218

Journal of China Pharmaceutical University > 2015 > 46(2): 242-249. > DOI: 10.11665/j.issn.1000-5048.20150218

GU Yi, LI Xiaoman, ZHENG Lufeng, YANG Jue, XI Tao. MicroRNA-10b regulates proliferation, cell cycle and apoptosis in human breast cancer cells[J]. Journal of China Pharmaceutical University, 2015, 46(2): 242-249. DOI: 10.11665/j.issn.1000-5048.20150218

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MicroRNA-10b regulates proliferation, cell cycle and apoptosis in human breast cancer cells

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To investigate the effects of miRNA-10b(miR-10b)on breast cancer proliferation and apoptosis in MCF-7 and MDA-MB-231, the miR-10b mimics used to increase the endogenous expression of miR-10b, and miR-10b inhibitor used to decrease the endogenous expression of miR-10b, were stably transfected into MCF-7 and MDA-MB-231 breast cancer cells. The expression level of miR-10b was determined by real-time PCR. The effects of miR-10b on proliferation were evaluated by MTT assay, while cell cycle assay and the apoptosis rate were measured by flow cytometry. Bioinformatic software was used to predict the potential targets of miR-10b, and 3′UTR luciferase reporter and qRT-PCR assay were used to verify a direct target of miR-10b. The expression levels of caspase-3 and p21 protein were measured by Western blot. Results confirmed that over-expression of miR-10b could promote the proliferation of breast cancer cells and inhibit the apoptosis by up-regulating the endogenous miR-10b, while the miR-10b inhibitor could restrain the proliferation of breast cancer cells and increase the apoptosis by reducing the endogenous miR-10b. In conclusion, miR-10b could negatively regulate the expression of caspase-3 and p21 by targeting TP53INP1, hence highlighting its potential as an oncogene in breast cancer cells.
- MicroRNA,
- miR-10b,
- breast cancer,
- proliferation,
- cell cycle,
- apoptosis,
- TP53INP1

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