Integrin α7 knockdown suppresses cell proliferation, migration, invasion and EMT in hepatocellular carcinoma.

Abstract

The present study aimed to investigate the effects of integrin α7 (ITGA7) on regulating hepatocellular carcinoma (HCC) progression and endothelial-mesenchymal transition (EMT). ITGA7 mRNA and protein expression in human normal liver epithelial cells and HCC cell lines were determined by reverse transcription-quantitative PCR (RT-qPCR) and western blotting. ITGA7 small interfering RNA [siRNA; ITGA7-knockdown (KD) group] and nonsense siRNA (control group) were transfected into Huh7 cells and SNU449 cells, respectively. ITGA7 mRNA and protein expression (RT-qPCR and western blotting, respectively), cell proliferation (Cell Counting Kit-8 assay), apoptosis (annexin V/propidium iodide assay), migration (wound scratch assay) and invasion (Transwell assay) were then detetected. E-cadherin, α-smooth muscle actin (α-SMA), vimentin and V-cadherin levels (RT-qPCR and western blotting) were also assessed. ITGA7 mRNA and protein expression levels were increased in Li7, Huh7, SKHEP1 and SNU449 cells compared with THLE-3 cells. Following transfection, ITGA7 mRNA and protein expression was lower in the ITGA7-KD group compared with that in the control group in both Huh7 and SNU449 cells, indicating successful transfection. In the ITGA7-KD group, cell proliferation decreased at 48 and 72 h, cell apoptosis rates increased at 48 h, cell migration rate was reduced at 24 h and cell invasion decreased at 24 h compared with the control group. Additionally, increased E-cadherin but decreased α-SMA, vimentin and V-cadherin mRNA and protein expression levels were observed in the ITGA7-KD group compared with the control group at 24 h. In conclusion, ITGA7 knockdown suppressed HCC progression and inhibited EMT in HCC in vitro, implying that ITGA7 might be a novel treatment target for HCC.