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

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. bound with the promoter of DDR1, and facilitated the phosphorylation of In turn, activation of duanyu18133 increased the expression of DDR1. Silencing of duanyu18133 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 duanyu18133 promoted HCC tumorigenesis. CONCLUSIONS:Our research revealed the positive feedback of DDR1 and duanyu18133 promoted EMT and glutamine metabolism in HCC, which provided some experimental basis for clinical treatment or prevention of HCC. MATERIALS AND METHODS:The mRNA expression of DDR1 was detected by qRT-PCR. CCK8 assay, wound healing assay and transwell assay were used to detect the DDR1/ duanyu18133 function on proliferation, migration and invasion in HCC cells. Western blot was used to calculate protein level of DDR1, epithelial-mesenchymal transition (EMT) related proteins.

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