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Liu et al. Hepatoma Res 2019;5:30  I  http://dx.doi.org/10.20517/2394-5079.2019.27                                                      Page 3 of 4

               of APOBEC3-signature HBV mutations and A1762T/G1764A in HBV-infected subjects, both of which
               were confirmed to associated with increased risk of HCC. The data of cohort studies demonstrated that
               APOBEC3B rs2267401-GG genotype, higher APOBEC3B expression, and higher APOBEC3B/UNG
               expression ratio in HCCs can predict a poor prognosis. Interestingly, APOBEC-signature somatic mutation
               predicts poor prognosis only in HBV-free HCC rather than in HBV-positive ones. These evidences strongly
               suggest that APOBEC3B facilitates HBV-induced HCC evolution via its mutagenic effect preferentially
               on the HBV genome. This result also explains why the APOBEC3-signature somatic mutation was not
                                       [11]
               dominant in HCC genome . APOBEC3B prefers to edit HBV genome possibly because the number of
               HBV genomic DNA is overwhelmingly more than that of human genome. Besides, during the replication
               of HBV, the partially double-stranded HBV DNA is generated from an intermediate RNA that is vulnerable
               to APOBEC3B.

               To conclude, the work by Wang and related studies demonstrated the important role of APOBEC3B in
               HCC evolution from different aspects. APOBEC3B promotes HBV-induced carcinogenesis through its
               mutagenic activity and facilitating immune escape of HCC through regulating epigenetic modification.
               The investigation for APOBEC3B can be transformed not only into specific prophylaxis but also into target
               therapy.


               DECLARATIONS
               Authors’ contributions
               Study concept and design: Cao GW
               Drafting of the manuscript: Liu WB
               Discussion and revision of the manuscript text: Cao GW

               Availability of Data and Materials
               Not applicable.

               Financial support and sponsorship
               This work was supported by grant (2015CB554006) from the National Key Basic Research Program of
               China (GC).

               Conflicts of interest
               All authors declared that there are no conflicts of interest.

               Ethical Approval and Consent to Participate
               Not applicable.

               Consent for publication
               Not applicable.

               Copyright
               © The Author(s) 2019.


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