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Hepatocellular carcinoma (HCC) is still a heavy threat to public health. However, novel therapeutic and diagnostic method for HCC is still urgently needed thus far. Based on sequence analysis and homology comparison, we previously reported a novel gene termed COMMD7, which is mapped to 20q11.22 and promotes cell proliferation in HCC cells. But the molecular mechanisms underlying the pro-tumor property of COMMD7 are not fully addressed yet. In this study, we demonstrate that the conditional medium derived from COMMD7-overexpressed HCC cell promotes proliferation of naïve HCC cells. The over-expression of COMMD7 significantly induced the migratory and invasive in HCC cells. Mechanistic study found that over-expression of COMMD7 induces C-X-C motif chemokine 10 (CXCL10) expression. Blocking CXCL10 signal transduction by neutralizing antibody abolished COMMD7-mediated cell proliferation and migration. In conclusion, COMMD7 promotes hepatocellular carcinoma through regulating CXCL10. The present data suggests a potential role of CXCL10 in the oncogenic function of COMMD7, and will lead to a better understanding of the development of HCC. Copyright © 2017 Elsevier Masson SAS. All rights reserved.


Nan You, Jing Li, Xiaobing Huang, Ke Wu, Yichen Tang, Liang Wang, Hongyan Li, Na Mi, Lu Zheng. COMMD7 promotes hepatocellular carcinoma through regulating CXCL10. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2017 Apr;88:653-657

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PMID: 28142122

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