Long non-coding RNA anti-differentiation non-coding RNA affects proliferation, invasion, and migration of breast cancer cells by targeting miR-331

Abstract

ABSTRACT We aimed to evaluate the effects of long-chain non-coding RNA (lncRNA) anti-differentiation non-coding RNA (ANCR) on the proliferation, invasion, and migration of breast cancer cells by targeting miR-331. Forty-eight breast cancer and paracancerous tissue samples were collected. LncRNA ANCR expressions in breast cancer and adjacent tissues, human breast cancer cells and mammary epithelial cells, and miR-331 expressions in interfering cell line MDA-MB-231 (MCF-7)-shANCR, negative control MDA-MB-231 (MCF-7)-shNC and blank control MDA-MB-231 (MCF-7) were detected by real-time quantitative PCR. The correlations between lncRNA ANCR expression and clinicopathological characteristics were analyzed. Cell proliferation was detected by MTT and colony formation assays. Invasion and migration were tested by Transwell and scratch assays, respectively. The targeting relationship between ANCR and miR-331 was analyzed using the TargetScan database, and their interaction was studied using a dual-luciferase reporter assay. The expression of lncRNA ANCR in breast cancer tissue was significantly lower than that in adjacent normal tissue (p < 0.05). LncRNA ANCR was lowly expressed in various human breast cancer cell lines, being lowest in high-metastatic cell line (MDA-MB-231HM) (p < 0.05). Silencing lncRNA ANCR significantly enhanced the proliferation and invasion capacities of breast cancer cells, and promoted their tumor formation abilities in nude mice (p < 0.05). ANCR bound miR-331 targetedly, and the former negatively regulated the expression of the latter. LncRNA ANCR is lowly expressed upon breast cancer, and inhibits cell proliferation, invasion, and migration in vitro and in vivo. LncRNA ANCR exerts antitumor effects by targetedly binding miR-331 and then inhibiting its expression.