Background & Aims: Linear ubiquitin chain assembly complex (LUBAC) has been reported to participate in cancer progression, but its role in hepatocellular carcinoma (HCC) remains unknown. This study aimed to investigate the functions and potential tumorigenic mechanisms of LUBAC components in HBV-associated HCC. Methods: The expression of LUBAC components ( RBCK1, RNF31, and Sharpin) and Met1-linked ubiquitination (M1-Ubi) and their correlation with prognosis were detected. The biological functions of RBCK1 in HBV-associated HCC were investigated in vitro and in vivo. The regulation of RBCK1 on the HBx protein expression was analyzed by cycloheximide chase assays, coimmunoprecipitation, and ubiquitin assays. Results: We found that the expression of LUBAC components and M1-Ubi was significantly upregulated in HCC and correlated with poor prognosis. Interestingly, subgroup analysis revealed that RBCK1, not RNF31 or Sharpin, was exclusively overexpressed in HBV-associated HCC compared to non-HBV-associated HCC. Upregulated RBCK1 expression was associated with larger tumor size, higher AFP level, and poor prognosis in HBV-associated HCC cohort. Functionally, RBCK1-knockdown suppressed cell growth and migration, and also inhibited the progression of xenografted tumors in HBV-associated HCC mouse model. Mechanistically, RBCK1 interacted with HBx to promote its stabilization by increasing M1-Ubi ubiquitination and reducing K48-linked ubiquitination. Furthermore, clinical analysis confirmed a positive correlation between RBCK1 and HBx, and the co-expression of which predicted poor prognosis for HCC patients. Conclusion: RBCK1 is an oncogenic gene to promote tumor progression and may serve as a potential target for HBV-associated HCC.