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NADPH oxidase 1 (NOX1)-mediated oxidative stress has been approved to contribute to carcinogenesis in a variety of tumors. However, the role of NOX1 in progression of hepatitis C virus (HCV)-induced hepatocellular carcinoma (HCC) and its relation to CXCR4 have not been fully elucidated.This is a retrospective study on 62 cases of HCV-induced HCC for assessment of the expression of NOX1 and CXCR4 by immunohistochemistry and to recognize their correlation with variable clinicopathological parameters.High NOX1 expression was detected in 43/62 (69.4%) of HCV-induced HCC and was significantly higher in HCC than adjacent nontumorous hepatitis tissues. NOX1 high expression was significantly correlated with high grade (P=0.004), TNM stage (P=0.009), and portal vein invasion (P=0.013). High NOX1 expression was detected in 23/62 (37.1%) of adjacent nontumorous hepatitis tissue and showed statistically significant correlation with inflammatory activity (P=0.007) and fibrosis (P=0.038) of Metavair scoring. CXCR4 expression was low, intermediate and high in 15/62 (24.2%), 22/62 (35.5%), and 25/62 (40.3%) of HCV-related HCC, respectively. High CXCR4 expression was significantly correlated with high grade (P=0.001), TNM stage (P=0.001), tumor multiplicity (P=0.008), and portal vein invasion (P=0.018). High significant positive correlation between NOX1 and CXCR4 immunoreactivity (P=0.009) was detected in HCC cases.The high expression of NOX1 and CXCR4 was associated with progression and aggressiveness of HCC. A significant association between NOX1 and CXCR4 might emphasize the crosstalk between chemokines and NOX1-mediated oxidative stress.