Repression of lncRNA-SVUGP2 mediated by EZH2 contributes to the development of non-small cell lung cancer via brisking Wnt/β-catenin signal.

To grab the possible impact of lncRNA-SVUGP2 in the biology and process of non-small cell lung cancer (NSCLC). Sixty paired NSCLC tumour and the adjacent non-tumour lung tissues were collected for detection of lncRNA-SVUGP2. lncRNA-SVUGP2 expression in NSCLC cells (SK-MES-1, A549, SPC-A1, and NCI-H1975) was also detected. lncRNA-SVUGP2 was overexpressed and depressed in A549 and H1975 cells, and the effects of lncRNA-SVUGP2 dysregulation on cell biological performances including viability, colony formation, apoptosis, migration and invasion were grabbed. Furthermore, the regulatory association of lncRNA-SVUGP2 vs. EZH2 in H1975 cells, as well as the association between lncRNASVUGP2 and Wnt/beta-catenin pathway, was explored. lncRNA-SVUGP2 was depressed in NSCLC tissues and cells. Overexpression of lncRNA-SVUGP2 depressed proliferation, induced apoptosis, and suppressed migration and invasion of A549 and H1975 cells. In addition, lncRNA-SVUGP2 was repressed by EZH2 and was inversely correlated with EZH2 levels in H1975 cells. Repression of lncRNA-SVUGP2 potentially participated in the oncogenic function of EZH2. Besides, overexpression of lncRNA-SVUGP2 depressed the briskness of Wnt/beta-catenin signal in H1975 cells. Our data reveal that lncRNA-SVUGP2 is under-expressed in NSCLC cells and the reduced expression of lncRNA-SVUGP2 may enhance the development and process of NSCLC by interacting with EZH2 and activating Wnt/beta-catenin pathway.