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Dai. Hepatoma Res 2019;5:33 Hepatoma Research
DOI: 10.20517/2394-5079.2019.26

Commentary Open Access

Comment on “APOBEC3B interaction with PRC2
modulates microenvironment to promote HCC

progression”

Beiying Dai

Center for New Drug Safety Evaluation and Research, State Key Laboratory of Natural Medicines, China Pharmaceutical
University, Nanjing 211198, Jiangsu, China.

Correspondence to: Prof. Beiying Dai, Center for New Drug Safety Evaluation and Research, State Key Laboratory of Natural
Medicines, China Pharmaceutical University, 639 Longmian Avenue, Nanjing 211198, Jiangsu, China.
E-mail: 1620184503@cpu.edu.cn

How to cite this article: Dai Beiying. Comment on “APOBEC3B interaction with PRC2 modulates microenvironment to promote
HCC progression”. Hepatoma Res 2019;5:33. http://dx.doi.org/10.20517/2394-5079.2019.26

Received: 11 Jul 2019 First Decision: 11 Jul 2019 Revised: 11 Jul 2019 Accepted: 12 Jul 2019 Published: 4 Sep 2019
Science Editor: Guang-Wen Cao Copy Editor: Cai-Hong Wang Production Editor: Jing Yu

Received: First Decision: Revised: Accepted: Published:
Accounting for 75%-85% of all primary liver cancer cases, hepatocellular carcinoma (HCC) is nowadays
Science Editor: Copy Editor: Production Editor: Jing Yu [1]
one leading cause of cancer-related mortality worldwide . More than half of HCC patients are diagnosed
at the advanced stage, for which limited treatment options are available and no curative ones exist so
[2]
far, leading to poor prognosis . The main risk factors for HCC, such as infection with HBV and HCV,
excessive alcohol consumption, obesity, and diabetes, all contribute to chronic liver inflammation, which
leads to the formation of an altered liver microenvironment. In turn, an altered liver microenvironment
can reciprocally reprogram the immune cells and hepatocytes involved in inflammation, together setting
[2-4]
the stage for progression to cirrhosis and eventually to HCC .

It has been demonstrated that tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells
(MDSCs) are the most abundant immune cell populations infiltrated in the tumor microenvironment of
HCC. As pivotal players in cancer-related inflammation, TAMs and MDSCs promote hepatocarcinogenesis
by stimulating angiogenesis and inducing immunosuppression and correlate with inferior prognosis .
[5-7]
Thus, it is of crucial importance to gain an in-depth look at the interplay between hepatocytes and immune
cells, especially TAMs and MDSCs, during the development of HCC.

[8]
Recently Wang et al. presented a remarkable study unraveling the functional significance of hepatocyte-
intrinsic apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3B [APOBEC3B (A3B)] in

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