Aberrant expression of LncRNA CASC2 mediated the cell viability, apoptosis and autophagy of colon cancer cells by sponging miR19a via NFB signaling pathway

Abnormal and rapid proliferation of colon cancer cells is a severe problem that can be regulated by noncoding RNAs. Thus, our study focused on effects of lncRNA CASC2 and miR19a on colon cancer cells. Expressions of lncRNA CASC2, miR19a, Bcl2, Bax and NFB/p65 were examined by RTqPCR. Cell viabilities were detected by CCK8. A luciferase report assay was used for measuring binding conditions between lncRNA CASC2 and miR19a. Western blotting was used to evaluate expression of LC3I, LC3II and p62 related to autophagy. Expression of lncRNA CASC2 lower in cancer cell lines and the overexpression reduced the cell viability of HT29 and SW480. Furthermore, Bcl2 was suppressed by overexpressed lncRNA CASC2, while Bax was upregulated. LC3 and p62 were both inhibited, but LC3 was promoted. MiR19a was predicted to bind lncRNA CASC2 and expressed higher in cancer cell lines. Overexpressed miR19a reduced expression of lncRNA CASC2 and increased cell viability. This was repressed by upregulated lncRNA CASC2. Bcl2 and Bax expression and proteins implicated in autophagy that are regulated by lncRNA CASC2 upregulation were reversed by miR19a overexpression. NFB was upregulated in colon cancer cell lines, while inhibition of NFB reversed functions of lncRNA CASC2 and magnified roles of miR19a. Our findings showed that lncRNA CASC2 inhibited cell viability in colon cancer cell lines and miR19a reversed its functions through the NFB signalling pathway, suggesting that these could be factors in treating colon cancer in the future.