Role of long non-coding RNA ENST 933 in breast cancer and its underlying mechanism

Abstract

Objective To investigate the regulatory mechanism of long non-coding RNA (lncRNA) ENST00000579933 (hereinafter referred to as lncRNA ENST 933) on the development of breast cancer (BC). Methods The expression level of lncRNA ENST 933 in BC tissues as well as in BC cell lines (MCF-7, MDA-MB-231, MDA-MB-453) was detected by fluorescence-based real-time quantitative polymerase chain reaction RT-qPCR. The effects of lncRNA ENST 933 and miR-588 on the proliferation, migration, invasion and cell cycle in BC were determined using CCK-8 assay, clone formation assay, EdU, Transwell assay, flow cytometry, Western blotting and in vivo transplantation tumor assay. Finally, dual luciferase reporter gene, RNA immunoprecipitation assay, RT-qPCR, Western blotting and rescue assay were used to evaluate the interactions among lncRNA ENST 933, miR-588, and eukaryotic initiation factor 6 (EIF6). Results The expression of lncRNA ENST 933 was up-regulated in both BC tissues and BC cell lines (P < 0.05). Overexpression of lncRNA ENST 933 could enhance the proliferation, migration and invasion abilities of BC cells and promote the growth of transplanted tumors, while knockdown of lncRNA ENST 933 resulted in inhibited development of BC and arrested cell cycle (P < 0.05). The expression of miR-588 was obviously down-regulated in BC tissues, and its overexpression inhibited cell proliferation, migration and invasion abilities in the BC cells (P < 0.05). Moreover, the results of rescue assay indicated that lncRNA ENST 933 promoted the expression of target gene EIF6 by competitively binding with miR-588. Western blotting revealed that miR-588 decreased the phosphorylation of AKT and mTOR (P < 0.05). Conclusion lncRNA ENST 933 promotes the progression of BC by modulating the miR-588/EIF6 axis.

Keywords

• enst00000579933
• mir-588
• eif6
• breast cancer
• proliferation
• invasion