Abstract
Objective: To explicit, the expression of chemokine receptor 3 in HCC tissues and its relationship with overall survival of patients, and to explore the effect of targeted silencing CXCR3 gene on proliferation of hepatocellular carcinoma cells and its mechanism of action. Methods: The expression of CXCR3 in 60 cases of hepatocellular carcinoma and its adjacent tissues were detected by immunohistochemistry. The clinicopathological correlations between the expression levels of CXCR3 in hepatoma tissues of liver cancer patients were analyzed and univariate Kaplan-Meier survival analysis was performed in combination with follow-up data. Huh7 hepatoma cells were infected with lentivirus LV-CXCR3-shRNA. The effects of CXCR3 deletion on proliferation of hepatoma cells were determined by CCK-8 assay and tumor-bearing nude mice experiment. Results: CXCR3 was highly expressed in HCC tissues, and the overall survival rate (OS) of patients with high CXCR3 expression was significantly lower than that of patients with low expression. After the CXCR3 gene was successfully silenced in Huh7 hepatocellular carcinoma cells, the proliferation ability of Huh7 cells was significantly inhibited in vitro, and the tumor growth rate of nude mice was slowed down, and the activity of JAK-STAT pathway in Huh7 cells was decreased, and the levels of c-MYC and Bcl-xl protein were decreased. In addition, deletion of CXCR3 can effectively inhibit IL-6-mediated JAK-STAT pathway activation. Conclusion: CXCR3 high expression indicated that the survival rate was poor, and the target silencing of CXCR3 gene could inhibit the proliferation of hepatocellular carcinoma cells and maybe related to inhibition of JAK-STAT pathway activity. CXCR3 may be a potential target for the treatment of hepatocellular carcinoma.