Abstract
LncRNAs exert comprehensive effects in regulating the initiation and deterioration of hepatocellular carcinoma (HCC). However, the specific expression profiles and functional mechanisms of LINC00536 in HCC need to be disclosed. The study is intended to clarify the leverage of LINC00536 in HCC and investigate the potential mechanisms for the regulatory role of LINC00536 in the progression of HCC. In our study, LINC00536 was overexpressed in tumor samples of HCC patients and was related to poor prognosis. LINC00536 knockdown impaired cell viability, proliferation, migration, and invasion. LINC00536 can directly bind with miR-203b-5p, trimming the miR-203b-5p expression levels. VEGFA designates as a target of miR-203b-5p. Rescue research indicated that the miR-203b-5p inhibition or VEGFA overexpression could reverse the impaired cell phenotypes induced by LINC00536 knockdown. The in vivo experiments upheld the LINC00536/miR-203b-5p/VEGFA axis in HCC. Conclusively, LINC00536 could promote HCC deterioration via tuning the miR-203b-5p/VEGFA axis. This research may provide theoretical evidence for LINC00536 to get a gratifying therapeutic target for HCC.