Inhibition of miR-214 attenuates the migration and invasion of triple-negative breast cancer cells

Triple-negative breast cancer (TNBC) is a subtype of breast cancer. MicroRNA (miR)-214 is closely associated with controlling the development of tumor cells; therefore, in the present study, the target gene and effects of miR-214 on TNBC cells were explored. Luciferase activity was examined by luciferase reporter assay. The viability, invasion and migration of MDA-MB-231 TNBC cells were measured using Cell Counting kit-8, Transwell and wound-healing assays, respectively. The expression levels of various factors were determined using reverse transcription-quantitative polymerase chain reaction and western blotting. The results demonstrated that the expression levels of miR-214 were higher and the levels of α1-antitrypsin (α1-AT) were lower in TNBC tissues compared with in normal tissues. Subsequently, α1-AT was revealed to be a target of miR-214. Furthermore, inhibition of miR-214 decreased cell viability, invasion and migration, enhanced the expression of E-cadherin and tissue inhibitor of metalloproteinases-2, and reduced the expression of metastatic tumour antigen 1 and matrix metalloproteinase-2. Inhibition of miR-214 also significantly downregulated the phosphorylation of protein kinase B (Akt) and mammalian target of rapamycin (mTOR), and markedly downregulated that of phosphoinositide 3-kinase (PI3K); however, the expression levels of total PI3K, Akt and mTOR remained stable in all groups. Taken together, these findings indicated that α1-AT may be a target of miR-214. Downregulation of miR-214 markedly suppressed the viability, migration and invasion of MDA-MB-231 cells, and inhibited the PI3K/Akt/mTOR pathway. These findings suggested that miR-214 targeting α1-AT may be a potential mechanism underlying TNBC development.