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Hepatitis B virus X protein plays a crucial role in the pathogenesis of hepatocellular carcinoma. We previously showed that the tumor suppressor  ARID 2 inhibits hepatoma cell cycle progression and tumor growth. Here, we evaluated whether hepatitis B virus X protein was involved in the modulation of  ARID 2 expression and hepatocarcinogenesis associated with hepatitis B virus infection.  ARID 2 expression was downregulated in  HBV ‐replicative hepatoma cells,  HBV  transgenic mice, and  HBV ‐related clinical  HCC  tissues. The expression levels of  HB x were negatively associated with those of  ARID 2 in hepatocellular carcinoma tissues. Furthermore,  HB x suppressed  ARID 2 at transcriptional level. Mechanistically, the promoter region of  ARID 2 gene inhibited by  HB x was located at nt‐1040/nt‐601 and contained potential  ATOH 1 binding elements. In addition, ectopic expression of  ATOH 1 or mutation of  ATOH 1 binding sites within  ARID 2 promoter partially abolished  HB x‐triggered  ARID 2 transcriptional repression. Functionally,  ARID 2 abrogated  HB x‐enhanced migration and proliferation of hepatoma cells, whereas depletion of  ATOH 1 enhanced tumorigenecity of  HCC  cells. Therefore, our findings suggested that deregulation of  ARID 2 by  HB x through  ATOH 1 may be involved in  HBV ‐related hepatocellular carcinoma development.

HB x protein‐mediated ATOH 1 downregulation suppresses ARID 2 expression and promotes hepatocellular carcinoma