The Role of lncRNA SNHG1 in Breast Cancer Cells by Targeting miRNA-101

Lei Zhu, Hong Chen, Ying Yang, Yan Miao, Jing Lu and JinKu Zhang

Background and Objective: Long non-coding RNA(lncRNA) is involved in various reactions in the body and is closely associated with drug resistance of breast cancer cells. The study was attempted to explore the target interaction of lncRNA SNHG1(SNHG1) and miR-101 in the mechanism of breast cancer progression. Materials and Methods: The breast cancer tissues and corresponding counterparts were collected. The expressions of SNHG1 and miR-101 in breast tumour tissues were elevated by qRT-PCR assay and the correlation was analyzed. The target interaction between SNHG1 and miR-101 was predicted by starbase online tool. MDA-MB-231 cells were subjected to co-transfection with SNHG1 shRNA and miR-101 inhibitors (sh-SNHG1 anti-miR-101) or SNHG1 shRNA and inhibitors control (sh-SNHG1 anti-NC). The changes in the proliferation, apoptosis, migrative and invasive ability of MDA-MB-231 cells was detected by MTT, flow cytometry and transwell assay, respectively. Western blot was performed to measure the protein expressions of cleaved Caspase-3 and MMP-2. Results: There was an inverse correlation between SNHG1 and miR-101 expression in breast cancer tissues. The binding site of SNHG1 in miR-101 was predicted. The luciferase activity of cells co-transfected with SNHG1-WT and miR-101 mimics was decreased. Meanwhile, the expression of miR-101 was pronouncedly elevated in cells of sh-SNHG1group. Compared with the sh-SNHG1 anti-NC group, cells co-transfected with sh-SNHG1and anti-miR-101 exhibited elevated cell proliferation, declined apoptosis rate and increased migrative and invasive ability of breast cancer cells. Parallelly, the activity of cleaved Caspase-3 was significantly reduced, while the MMP-2 level was significantly elevated in the sh-SNHG1 anti-miR-101 group. Conclusion: SNHG1 increased the development and metastasis of breast cancer cells by negatively regulating miR-101 expression.

View Fulltext Back