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

Abstract

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.

The uprise of RNA biology in neuroendocrine neoplasms: altered splicing and RNA species unveil translational opportunities

“…In SCLC, this phenomenon was well studied, as is the case HOTTIP , a lncRNA overexpressed in SCLC samples, where it correlates with tumor stage and shorter overall survival. HOTTIP works as a miR-574-5p sponge, regulating the expression of histone methylase EZH1 [ 109 ] and also regulating epithelial-mesenchymal transition [ 110 ]. HOTTIP may also sponge miR-216a, thus increasing the expression of the antiapoptotic protein BCL2 and enhancing chemoresistance, as miR-216a is correlated with good prognosis and suppresses chemoresistance [ 111 ].…”

Potential microRNA biomarker panel for predicting evolution of pancreatitis to pancreatic ductal adenocarcinoma

“…Group 1 included hsa-miR-574-5p and 608 Hsa-miR-574-5p, is known to be involved in fatty acid elongation, base excision repair, hippo signaling pathway, lysine degradation, purine metabolism, and viral carcinogenesis [15]. It is known to be involved in lung adenocarcinoma, small cell lung cancer, breast cancer, gastric cancer, and nasopharyngeal cancer [16, 17,18,19,20,21]. It is also involved in other in ammatory pathways including diabetes, asthma, and cardiac remodeling [22,23,24,25].…”