lncRNAs are responsible for a variety of diseases, including gastric cancer (GC). Many recent studies have reported that lncRNAs can serve as crucial regulators of various genes. Nevertheless, the biological function of lncRNA damage induced noncoding (DINO) remained poorly investigated in GC. Therefore, in our present study, the detailed role of DINO was investigated. It was manifested that DINO was significantly downregulated in GC tissues. Then, DINO was modulated by infecting LV-DINO or by LV-shRNA in BGC-823 and MGC-803 cells. Moreover, it was displayed that GC cell proliferation was suppressed by DINO overexpression, whereas silencing DINO increased cell proliferation significantly. For another, it was indicated that DINO dramatically induced apoptotic ratios of BGC-823 and MGC-803 cells, whereas the decrease of DINO depressed GC cell apoptosis. Apart from these, GC cell cycle progression was greatly blocked by LV-DINO. Furthermore, Western blot results displayed that upregulation of DINO elevated p21 expression and Bax expression. Oppositely, inhibition of DINO greatly suppressed p21 and Bax protein expression level. Taken these, DINO might exert a tumor inhibitory role in the progression of GC through modulating p21 and Bax.
Keywords: Bax; damage induced noncoding (DINO); gastric cancer (GC); p21.
© 2019 Wiley Periodicals, Inc.