Long intergenic noncoding RNA smad7 (Linc-smad7) promotes the epithelial-mesenchymal transition of HCC by targeting the miR-125b/SIRT6 axis.

Abstract

Long intergenic noncoding RNA smad7 (Linc‐smad7) has been recently identified as a new long non‐coding RNA (lncRNA). However, the role of Linc‐smad7 in the tumourigenesis of human cancers remains unknown. This study uncovered that Linc‐smad7 was increased in HCC samples and HCC cell lines using RT‐qPCR assays. Furthermore, the overexpression of Linc‐smad7 indicated poor clinicopathological features and outcomes for HCC patients. In addition, Linc‐smad7 promoted HCC cells proliferation, migration, invasion and EMT, as determined by MTT, colony formation, Transwell assays and western blot analysis. Functionally, it was demonstrated that Linc‐smad7 could bind with microRNA‑125b (miR‑125b), and the restoration of miR‑125b rescued the promoting effects of Linc‐smad7 on HCC cells. Finally, it was observed that sirtuin 6 (SIRT6) was positively regulated by Linc‐smad7 in HCC as the direct target of miR‑125b, and decreased SIRT6 reversed the effects of Linc‐smad7 on promoting HCC. In conclusion, the current study first identified Linc‐smad7 is increased in HCC, facilitating HCC cells proliferation, migration, invasion and EMT via regulating the miR‑125b/SIRT6 axis.