MicroRNA-27a promotes tumorigenesis via targeting AKT in triple negative breast cancer

Altered microRNA (miRNA/miR) expression regulates tumor development and progression in triple-negative breast cancer (TNBC). The present study examined the effect of miR-27a on proliferation, migration and invasion of TNBC cells in vitro and in vivo. An MTT assay was performed to examine the proliferation of MDA-MB-231 and MDA-MB-468 breast cancer cells with either overexpression of miR-27a or downregulation of miR-27a, in the presence or absence of radiation. The migratory and invasive abilities of MDA-MB-231 and MDA-MB-468 breast cancer cells were assessed by Transwell migration and Matrigel invasion assays. The protein expression levels were examined by western blotting. The caspase-Glo3/7 assay was performed to examine the effect of miR-27a on radiation-induced apoptosis in MDA-MB-231 and MDA-MB-468 breast cancer cells. A luciferase assay was performed to evaluate the effect of miR-27a on phosphatase and tensin homolog (PTEN) and B cell lymphoma (Bcl)-2 associated X, apoptosis regulator (BAX) expression. Immunodeficient nude mice were used to examine tumor growth following injection of MDA-MB-231 breast cancer cells. miR-27a promoted proliferation in vitro and in vivo, and enhanced migration and invasion in TNBC cells. miR-27a improved the survival of TNBC cells following irradiation. miR-27a inhibited radiation-induced apoptosis in TNBC cells by regulation of caspase 3/7 and Bcl-2 expression. Furthermore, the expression levels of PTEN and phosphorylated protein kinase B in MDA-MB-231 and MDA-MB-468 cells was altered following overexpression of miR-27a. The luciferase assay demonstrated that miR-27a regulated PTEN and BAX expression by binding to 3-untranslated regions. Overall, miR-27a exhibits an essential role in tumor development and progression in TNBC and may be used as a potential biomarker to predict radiotherapy response and prognosis for the disease.