CD24–p53 axis suppresses diethylnitrosamine-induced hepatocellular carcinogenesis by sustaining intrahepatic macrophages View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-02-06

AUTHORS

Dongling Li, Minling Hu, Ying Liu, Peiying Ye, Peishuang Du, Chi-Shan Li, Liang Cheng, Ping Liu, Jing Jiang, Lishan Su, Shengdian Wang, Pan Zheng, Yang Liu

ABSTRACT

It is generally assumed that inflammation following diethylnitrosamine (DEN) treatment promotes development of hepatocellular carcinoma (HCC) through the activity of intrahepatic macrophages. However, the tumor-promoting function of macrophages in the model has not been confirmed by either macrophage depletion or selective gene depletion in macrophages. Here we show that targeted mutation of Cd24 dramatically increased HCC burden while reducing intrahepatic macrophages and DEN-induced hepatocyte apoptosis. Depletion of macrophages also increased HCC burden and reduced hepatocyte apoptosis, thus establishing macrophages as an innate effector recognizing DEN-induced damaged hepatocytes. Mechanistically, Cd24 deficiency increased the levels of p53 in macrophages, resulting in their depletion in Cd24-/- mice following DEN treatment. These data demonstrate that the Cd24-p53 axis maintains intrahepatic macrophages, which can remove hepatocytes with DNA damage. Our data establish a critical role for macrophages in suppressing HCC development and call for an appraisal of the current dogma that intrahepatic macrophages promote HCC development. More... »

PAGES

6

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41421-017-0007-9

DOI

http://dx.doi.org/10.1038/s41421-017-0007-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1100795955

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29423273


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