The cross-talk between DDR1 and STAT3 promotes the development of hepatocellular carcinoma.

ABSTRACT:

Objective

To investigate the function of discoidin domain receptor 1 (DDR1) in hepatocellular carcinoma (HCC) and to further clarify the underlying mechanism.

Results

DDR1 was significantly increased in HCC tissues and cells, which was related to clinical staging and prognosis of HCC. Upregulation of DDR1 promoted EMT and glutamine metabolism in HCC cells, while loss of DDR1 showed the opposite effects. STAT3 bound with the promoter of DDR1, and facilitated the phosphorylation of STAT3. In turn, activation of STAT3 increased the expression of DDR1. Silencing of STAT3 removed the promoting effect of DDR1 on proliferation, migration and invasion of HCC cells. The in vivo tumor growth assay showed that the cross-talk between DDR1 and STAT3 promoted HCC tumorigenesis.

Conclus

SUBMITTER: Lin Y 

PROVIDER: S-EPMC7425490 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature