miR-574-5p mediates epithelial-mesenchymal transition in small cell lung cancer by targeting vimentin via a competitive endogenous RNA network.

Numerous studies have suggested that non-coding RNAs mediate tumorigenesis via the epithelial-mesenchymal transition (EMT). However, whether the long non-coding RNA (lncRNA) HOXA transcript at the distal tip (HOTTIP) plays a role in the EMT of small cell lung cancer (SCLC) remains unclear. The results of the present study suggest that HOTTIP-knockdown may lead to a significant increase in E-cadherin expression and a decrease in vimentin (VIM) expression; these proteins are two key markers of EMT. Furthermore, a notable morphological change in SCLC cells with HOTTIP-knockdown was observed: After upregulation of microRNA (miR)-574-5p, the cells exhibited a long, fusiform morphology. Investigating these phenomena further revealed that HOTTIP may participate in EMT by binding to miR-574-5p. In addition, using bioinformatics technology and a dual luciferase reporter assay, it was found that miR-574-5p inhibited VIM expression via direct binding and interaction. In summary, the present results indicate that HOTTIP may be involved in the EMT of SCLC by binding to miR-574-5p, and that miR-574-5p may act through VIM, which is a key marker of EMT.