Abstract：
:Inflammation predisposes to tumorigenesis in various organs by potentiating a susceptibility to genetic aberrations. The mechanism underlying the enhanced genetic instability through chronic inflammation, however, is not clear. Here, we demonstrated that TNFα stimulation induced transcriptional downregulation of MSH2, a member of the mismatch repair family, via NF-κB-dependent miR-21 expression in hepatocytes. Liver cancers developed in ALB-MSH2(-) (/) (-)AID(+), ALB-MSH2(-) (/) (-), and ALB-AID(+) mice, in which MSH2 is deficient and/or activation-induced cytidine deaminase (AICDA) is expressed in cells with albumin-producing hepatocytes. The mutation signatures in the tumors developed in these models, especially ALB-MSH2(-) (/) (-)AID(+) mice, closely resembled those of human hepatocellular carcinoma. Our findings demonstrated that inflammation-mediated dysregulation of MSH2 may be a mechanism of genetic alterations during hepatocarcinogenesis. Cancer Res; 76(15); 4383-93. ©2016 AACR.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Eso Y,Takai A,Matsumoto T,Inuzuka T,Horie T,Ono K,Uemoto S,Lee K,Edelmann W,Chiba T,Marusawa Hdoi
10.1158/0008-5472.CAN-15-2926subject
Has Abstractpub_date
2016-08-01 00:00:00pages
4383-93issue
15eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-15-2926journal_volume
76pub_type
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