关键词: lncRNA VIM-AS5, 乳腺癌, miR-500a, 细胞增殖, 细胞迁移

Abstract: Objective To explore the clinical significance of long non-coding RNA(lncRNA) VIM-AS5 expression in human breast cancer tissues and its regulatory mechanism involved in cancer cell proliferation and migration. Methods The Lnc2Cancer 3.0 database was used to analyze the expression of VIM-AS5 in breast cancer tissues and its correlation with the clinical stage and survival time of breast cancer patients. RT-qPCR was used to detect the expression of VIM-AS5 in breast cancer cell lines BT-549, MDA-MB-435, MDA-MB-231 and CAL-51. Plasmid with VIM-AS5 overexpression and negative control were all transfected into CAL-51 cells through liposome recorded as VIM-AS5 group and NC group, respectively. The proliferation and migration of CAL-51 cells were detected by colony formation assay and scratch healing method, respectively. Dual-luciferase reporter gene experiment verified the targeting relationship between VIM-AS5 and miR-500a. RT-qPCR was used to detect the expression of miR-500a in CAL-51 cells. Western blot was used to detect the expression of JAK/STAT3 pathway in CAL-51 cells. Results The expression of VIM-AS5 in breast cancer tissues was significantly lower than that in adjacent tissues(P＜0.01). VIM-AS5 expression was negatively correlated with the clinical stage of breast cancer patients(P＜0.01). The survival time of breast cancer patients with low VIM-AS5 expression was significantly shorter than that of breast cancer patients with high VIM-AS5 expression(P＜0.01). Compared with mammary epithelial cell line MCF-10A cells, VIM-AS5 expression was significantly reduced in breast cancer cells(P＜0.01). The counting number of colony formed in the VIM-AS5 group was significantly lower than that in the NC group(P＜0.01). The cell migration rate in the VIM-AS5 group was significantly lower than that in the NC group(P＜0.01). Dual-luciferase reporter gene experiment confirmed that miR-500a was the target gene of VIM-AS5(P＜0.01). VIM-AS5 can negatively regulate the expression of miR-500a(P＜0.01). Compared with the NC group, the expression of JAK/STAT3 pathway proteins JAK, p-STAT3, c-Myc, Bcl-2, and CDK3 in CAL-51 cells of the VIM-AS5 group were significantly decreased. Conclusions VIM-AS5 is low-expressed in breast cancer cells, and up-regulation of VIM-AS5 may inhibit the proliferation and migration of breast cancer cells CAL-51 by targeting at miR-500a/JAK/STAT3 pathway.

Key words: lncRNA VIM-AS5, breast cancer, miR-500a, cell proliferation, cell migration