LncRNA OIP5-AS1 Upregulates the Cyclin D2 Levels to Promote Metastasis of Breast Cancer by Targeting miR-150-5p

Objective Breast cancer (BC) is a cancer that seriously affects women's health. BC cell migration increases the mortality of BC patients. Current studies have shown that long noncoding RNAs (LncRNAs) are related to the metastasis mechanism of BC. This study aimed to explore the function and role of LncRNA OIP5-AS1 in BC. And we analyzed its regulatory mechanism and related modification process. Methods Our study analyzed the expression pattern of OIP5-AS1 in BC tissues and cell lines by qRT-PCR. The effects of OIP5-AS1 on the function of BC cells were detected by CCK-8 and transwell experiments. Bioinformatics analysis and double luciferase reporter gene detection were used to confirm the correlation between OIP5-AS1 and miR-150-5p and between miR-150-5p and Cyclin D2 (CCND2). The rescue test analyzed the effect of miR-150-5p regulating OIP5-AS1. In addition, the N-6-methyladenosine (m(6)A) modification process of OIP5-AS1 was analyzed by RNA m(6)A dot blot, RIP assay, and double luciferase report experiment. Results OIP5-AS1 was significantly upregulated in BC tissues and cell lines. OIP5-AS1 knockdown inhibited BC cell viability, migration and invasion. OIP5-AS1 upregulated CCND2 by binding with miR-150-5p. This process affected the metastasis of BC. Higher degree of m(6)A methylation was confirmed in BC cell lines. There were some binding sites between methyltransferase like 3 (METTL3) and OIP5-AS1. Moreover, the silencing of METTL3 inhibited the OIP5-AS1 expression through decreasing the m(6)A methylation levels. Conclusions LncRNA OIP5-AS1 promoted cell viability and metastasis of BC cells by targeting miR-150-5p/CCND2 axis. This process was modified by m(6)A methylation of METTL3.