MiR-346 promotes the biological function of breast cancer cells by targeting SRCIN1 and reduces chemosensitivity to docetaxel.

ABSTRACT

MicroRNAs (miRNAs) are a class of highly conserved small noncoding RNAs that play pivotal roles at the post-transcriptional level in the biological function of various cancers, including breast cancer. In our study, miR-346 mimic, inhibitor, negative control or si-SRCIN1 were transfected into MCF-7 and MCF-7/Doc cells, respectively. Quantitative real time PCR (qRT-PCR) was used to measure miR-346 and SRCIN1 mRNA expressions and western blot was used to detect the expression of SRCIN1 in protein level. CCK-8 and colony formation were employed to verify cell viability and proliferation. Flow cytometry showed the apoptosis. Transwell was performed to detect migration and invasion. The luciferase reporter assay data showed the target correlation of miR-346 and SRCIN1. Firstly, we found that the expression of miR-346 was higher in breast cancer tissues than in their paired corresponding non-cancerous tissues and there was significant inversed correlation between miR-346 and SRCIN1. Overexpression of miR-346 promoted cell proliferation, colony formation, migration and invasion, and reduced apoptosis, sensitivity to Docetaxel (Doc). SRCIN1 was identified as a direct target of miR-346, whose silencing promoted cell proliferation and the IC50 of Doc. Moreover, SRCIN1 silencing reduced the effect of miR-346 down-expression. Taken together, miR-346 may function as an oncogenic miRNA and mediate chemosensitivity to docetaxel through targeting SRCIN1 in breast cancer, targeted modulation of miR-346 expression may became a potential strategy for the treatment.