LncRNA UCC promotes epithelial-mesenchymal transition via the miR-143-3p/SOX5 axis in non-small-cell lung cancer

Long non-coding RNAs (lncRNAs) have been found to play regulatory roles in cancers; for example, UCC was reported to promote colorectal cancer progression. However, the function of UCC in non-small-cell lung cancer (NSCLC) remains unclear. Therefore, mRNA and protein levels were assessed using qPCR and western blots. Cell viability was assessed by colony-formation assays. The interaction between lncRNAs and miRNAs was detected by dual-luciferase reporter and RIP assays. The tumorigenesis of NSCLC cells in vivo was determined by xenograft assays. LncRNA UCC was highly expressed in both NSCLC tissues and cells. Knockdown of UCC expression suppressed the proliferation of NSCLC cells. In addition, a dual-luciferase reporter system and RIP assays showed that UCC specifically bound to miR-143-3p and acted as a sponge of miR-143-3p in NSCLC cells. The miR-143-3p inhibitor rescued the inhibitory effect of sh-UCC on the proliferation of NSCLC cells. Moreover, miR-143-3p and UCC showed opposite effects on the expression of SOX5, which promoted EMT in NSCLC cells. In addition, in a mouse model, knockdown of UCC expression alleviated EMT and NSCLC progression in vivo, which was consistent with the in vitro results. In the current study, we found that UCC induced the proliferation and migration of NSCLC cells both in vitro and in vivo by inducing the expression of SOX5 via miR-143-3p and subsequently promoted EMT in NSCLC. The long non-coding RNA UCC acts as a competing endogenous RNA of miR-143-3p and upregulates SOX5 by absorbing miR-143-3p, resulting in proliferation and migration of non-small-cell lung cancer (NSCLC) cells both in vitro and in vivo. UCC enhances carcinogenesis of NSCLC cells via the miR-143-3p/SOX5 axis, which may function as a novel target for NSCLC treatment.