[No authors listed]
While >80% of the incidence occurs in subâSaharan Africa and East Asia, cases of hepatocellular carcinoma (HCC) have been rapidly increasing in Western countries. Despite its global importance, HCC is relatively underâresearched compared with other lethal cancer types, which is possibly due to the high complexity and heterogeneity of HCC. It has been reported previously that COMM domainâcontaining protein 7 (COMMD7) is upregulated in HCC and promotes HCC cell proliferation by triggering CâXâC motif chemokine 10 (CXCL10) production. However, the value of targeting CXCL10 signal transduction in treating COMMD7âpositive tumors, or the molecular mechanisms underlying COMMD7âmediated CXCL10 expression, has not been completely addressed. In the present study, it was demonstrated that disruption of the CXCL10/CâXâC chemokine receptor type 3 axis reduces COMMD7âmediated HCC cell proliferation. Furthermore, COMMD7 modulates CXCL10 production by activating nuclear factor (NF)âκB. Additionally, it was demonstrated that intracellular reactive oxygen species are required for NFâκB activation and CXCL10 production. In conclusion, COMMD7 activates CXCL10 production by regulating NFâκB and the production of The present study highlighted the role of COMMD7 in the development of HCC, and provides novel options for anticancer drug design.
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