High expression of lncRNA MEG3 participates in non-small cell lung cancer by regulating microRNA-7-5p.

Abstract

This study was made to investigate whether long noncoding RNA (lncRNA) MEG3 could participate in the occurrence and development of non-small cell lung cancer (NSCLC) by regulating the expression of BRCA1 through competitive binding to microRNA-7-5p. We used quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) to explore the expression of lncRNA MEG3 and BRCA1 in NSCLC tissues and adjacent normal tissues, as well as NSCLC cell lines. The dual luciferase reporter gene assay was used to detect the binding of microRNA-7-5p to lncRNA MEG3 and BRCA1. Meanwhile, the expression of BRCA1, B-cell lymphoma-2 (Bcl-2) and BCL2-associated X (Bax) was detected by Western blot after the cells were overexpressed or knocked down of lncRNA MEG3. All these experiments were designed to investigate whether lncRNA MEG3 participated in the pathogenesis of NSCLC through inhibiting the expression of BRCA1 and Bcl-2 and promoting Bax expression. The expressions of lncRNA MEG3 and BRCA1 in NSCLC tissues and A549 and HCC823 cell lines were significantly lower than those in the normal group. Overexpression of lncRNA MEG3 and BRCA1 in A549 and HCC823 cell lines resulted in increased apoptosis of lung cancer cells. Dual luciferase reporter assay demonstrated that lncRNA MEG3 can regulate the expression of BRCA1 through competitively binding to microRNA-7-5p to form the lncRNA MEG3/microRNA-7-5p/BRCA1 regulatory network. Besides, lncRNA MEG3 could inhibit the apoptosis inhibitory protein Bcl-2 and promote the expression of apoptosis-promoting factor Bax. LncRNA MEG3 was significantly downregulated in NSCLC, and it could regulate the BRCA1 expression by competitive binding to microRNA-7-5p.