MiR-214-3p regulates the viability, invasion, migration and EMT of TNBC cells by targeting ST6GAL1.

Abstract

MiR-214-3p is concerned with the outcomes of various tumors, such as liver cancer, bladder cancer, etc. However, the role and target of miR-214-3p in triple negative breast cancer (TNBC) is not fully understood. This study took this as the entry point, with a view to find a potential target for TNBC. The expressions of miR-214-3p in TNBC tissues and cell lines were detected, and the effects of miR-214-3p inhibitor on the viability, migration, invasion and epithelial mesenchymal transition (EMT) of TNBC cells were further analyzed. The potential target of miR-214-3p were predicted and verified, as well as the effects of target silencing on the TNBC cells were also measured. MiR-214-3p was abnormally elevated in both TNBC tissues and cell lines, especially in MDA-MB-468 cells. Low-expression of miR-214-3p restrained the survival, migration, invasion and EMT of TNBC cells. ST6GAL1 was the target gene of miR-214-3p, and its expression level increased with the low-expression of miR-214-3p. ST6GAL1 expression was abnormally reduced in both TNBC tissues and cell lines. The silence of ST6GAL1 promoted the viability, migration, invasion and EMT of TNBC cells, which could be reversed by miR-214-3p inhibitor. The down-regulation of miR-214-3p could suppress the viability, migration, invasion and EMT of TNBC cells though targeting ST6GAL1, which might be a potential target for future treatment of TNBC. Up-regulation of miR-214-3p could promote the EMT of non-TNBC cells.