ABSTRACT
@#[Abstract] Objective: To investigate the effect of lncRNA SNHG15 targeting miR-153 on cell viability and apoptosis of breast cancer cells and its apoptotic mechanism. Methods:The expression of SNHG15 in breast cancer cell lines(MDA-MB-231, BT-549 and MCF-7) were detected by Real-time fluorescent quantitative PCR (qPCR). MDA-MB-231 cells were divided into control (Ctrl) group, si-NC group, si-SNHG15 group, si-SNHG15+anti-NC group and si-SNHG15+anti-miR-153 group. Cell viability and apoptosis rate were detected by MTT and Flow cytometry, respectively. The targeting relationship between SNHG15 and miR-153 was verified by Dual luciferase report gene system. Mitochondrial membrane potential fluorescent probe (JC-1) staining method was used to detect cell mitochondrial membrane potential. The expressions of mitochondrial apoptosis-related proteins (Bcl-2, Bax, caspase3, cleaved caspase3 [c-caspase3] and Cyt-C）were detected by Western blotting. Results: The expression of SNHG15 in breast cancer cells was significantly higher than that in human normal mammary epithelial MCF10A cells (P<0.01). There was a targeting relationship between SNHG15 and miR-153. Compared with the control group, the cell viability and mitochondrial membrane potential of MDA-MB-231 cells in si-SNHG15 group were decreased, while apoptosis rate was increased (all P<0.01); the expressions of Bcl-2 and caspase3 were decreased while expressions of Bax, c-caspase3 and Cyt-C were increased (all P<0.01). However, co-transfection of si-SNHG15 and anti-miR-153 significantly attenuated the effects of si-SNHG15 on cell viability, apoptosis, mitochondrial membrane potential and expressions of Bcl-2, Bax, caspase3, c-caspase3 and Cyt-C (all P<0.01). Conclusion: lncRNA SNHG15 can target miR-153 to induce apoptosis of MDA-MB-231 cells, and the mechanism may be related to the regulation of apoptosis of mitochondrial pathway.