Background
Breast cancer (BC) is a common cancer with high incidence in women worldwide. Although there are some studies focusing on the pathogenesis of BC, the regulatory mechanism needs to be further investigated. The function of lncRNA and miRNA has been demonstrated to participate in cell progression of BC. However, the function of SNHG12 has not been clearly elucidated.
Conclusion
Knockdown of SNHG12 inhibited cell proliferation, invasion, and migration by regulating miR-451a through suppression of AKT/mTOR pathway in BC.
Methods
We detected the expression of SNHG12 and miR-451a using quantitative real-time PCR (qRT-PCR). The protein expression of AKT, p-AKT, mTOR and p-mTOR were measured using western blot. The relationship between SNHG12 and miR-451a was confirmed by luciferase reporter assay. Cell proliferation was measured using MTT assay. Transwell assay was used to detect cell migration and invasion. Xenograft transplantation was used to detect the function of SNHG12 in vivo.
Results
In this study, we found that SNHG12 was significantly increased in BC tissues and cells. Knockdown of SNHG12 inhibited BC cell proliferation, invasion, and migration in vitro as well as suppressed tumor growth in vivo. In addition, miR-451a expression was obviously down-regulated in BC tissues and had negative correlation with SNHG12. Luciferase reporter assay determined that miR-451a was a target miRNA of SNHG12. Notably, SNHG12 knockdown decreased cell proliferation, migration, invasion, and AKT/mTOR pathway activation which could be reversed by down-regulation of miR-451a.