Long non-coding RNA ZEB2-AS1 promotes proliferation and inhibits apoptosis in human lung cancer cells.

Lung cancer is among the leading causes of cancer-associated mortality worldwide, with a low 5-year survival rate of 16.1%. However, the underlying molecular mechanisms behind lung cancer tumorigenesis remain largely unknown. Long non-coding RNAs (lncRNAs) have been demonstrated to serve a function in the tumorigenesis of multiple types of cancer. The objective of the present study was to identify the function of a newly identified lncRNA zinc finger E-box-binding homeobox 2 antisense RNA 1 (ZEB2-AS1) in human lung cancer. Results demonstrated that the transcript level of ZEB2-AS1 in human lung cancer was markedly upregulated in vivo and in vitro. The knockdown of ZEB2-AS1 in A549 and NCI-H292 cells, and the overexpression of ZEB2-AS1 in H-125 and H1975 cells, altered colony formation and cell proliferative rate, as examined using colony formation and cell proliferation assays. Western blot analysis revealed that the knockdown of ZEB2-AS1 in A549 and NCI-H292 cells increased the protein levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3 and -9, upregulated the relative activities of caspase-3 and -9, and had no observable effect on caspase-8 activity. Similarly, the overexpression of ZEB2-AS1 in H-125 and H1975 cells resulted in decreased expression of caspase-3, caspase-9, Bcl-2 and Bax. The results identified the effects of lncRNA ZEB2-AS1 on lung cancer progression through promoting its proliferation and inhibiting cell apoptosis, indicating that ZEB2-AS1 may serve as a novel prognostic factor for the diagnosis and treatment of human lung cancer in the clinic.