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.