TATDN1 promotes the development and progression of breast cancer by targeting microRNA-140-3p.

Abstract

To explore whether long non-coding RNA (lncRNA) TATDN1 can promote the proliferation and cell cycle progression of breast cancer cells by adsorbing microRNA-140-3p, thus participating in the development of breast cancer (BCa). Expressions of TATDN1 and microRNA-140-3p in BCa tissues and paracancerous tissues were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Meanwhile, TATDN1 expression in BCa cell lines was detected as well. Regulatory effects of TATDN1 and microRNA-140-3p on proliferation and cell cycle progression of BCa cells were evaluated by Cell Counting Kit-8 (CCK-8) and flow cytometry, respectively. The binding relationship of microRNA-140-3p to NOVA1 and TATDN1 was examined by dual-luciferase reporter gene assay. Finally, rescue experiments were conducted to explore whether TATDN1 can regulate NOVA1 expression by adsorbing microRNA-140-3p to exert its biological function in BCa. TATDN1 was highly expressed in BCa tissues and cell lines. Upregulation of TATDN1 promoted the proliferative potential and cell cycle progression of MCF-7 and MDA-MB-231 cells. Dual-luciferase reporter gene assay indicated that TATDN1 could bind to microRNA-140-3p, which was lowly expressed in BCa. Overexpression of microRNA-140-3p inhibited the proliferative potential and cell cycle progression of MCF-7 and MDA-MB-231 cells. Moreover, microRNA-140-3p partially inhibited the role of TATDN1 in regulating cellular behaviors of BCa cells. NOVA1 was predicted to be the target gene of microRNA-140-3p. Overexpression of NOVA1 partially abolished the inhibitory effects of microRNA-140-3p on proliferation and cell cycle progression of MCF-7 and MDA-MB-231 cells. TATDN1 promotes the proliferative potential and cell cycle progression of BCa cells through adsorbing microRNA-140-3p to upregulate NOVA1 expression.