Abstract
OBJECTIVE: To analyze the association of integrinα5 (ITGA5) with grading of liver cancer and the overall patient survival and investigate the effects of integrin α5 (ITGA5) silencing on the proliferation, invasion and migration abilities of human liver cancer Bel-7404 cells. METHODS: UALCAN was used to analyze the expression of ITGA5 in liver cancer tissues and normal tissues, and expression in different grades of liver cancer tissues. GEPIA was used to analyze the relationship between ITGA5 expression and the survival of liver cancer patients through.The ITGA5 shRNA lentiviral vector was used to infect Bel-7404 cells to establish a cell line with stable ITGA5 silencing verified by Western blotting. Plate clone formation assay and Transwell assay were used to detect the proliferation, invasion and migration of Bel-7404 cells. The correlation between ITGA5 and PI3K in liver cancer tissues and control tissues was analyzed using Oncomine cancer specimen database. RESULTS: The expression of ITGA5 was significantly higher in liver cancer than in normal tissues (P < 0.05). The expression of ITGA5 was significantly lower in grade 1 than in grade 2 liver cancer, and also lower in grade 2 than in grade 3 liver cancer (P < 0.05). The patients with high ITGA5 expression had a significantly lower overall survival rate than those with low ITGA5 expression (P < 0.05). Plate clone formation assay showed that the clone formation rate was significantly lowered in Bel-7404 cells with ITGA5 silencing compared with the blank and negative control cells (P < 0.05). ITGA5 silencing significantly attenuated the migration of Bel-7404 cells as shown by Transwell assay (P < 0.05). ITGA5 and PI3K were both highly expressed and showed a positive correlation in liver cancer tissues (P < 0.05). CONCLUSIONS: ITGA5 is closely related to the progression of liver cancer and the patients' prognosis. ITGA5 silencing inhibits the proliferation, invasion and migration of liver cancer cells. ITGA5 promotes the liver cancer growth and metastasis possibly by regulating the PI3K signaling pathway.