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COMMD7 promotes hepatocellular carcinoma through regulating CXCL10.

Authors :
You N
Li J
Huang X
Wu K
Tang Y
Wang L
Li H
Mi N
Zheng L
Source :
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [Biomed Pharmacother] 2017 Apr; Vol. 88, pp. 653-657. Date of Electronic Publication: 2017 Jan 29.
Publication Year :
2017

Abstract

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.<br /> (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)

Details

Language :
English
ISSN :
1950-6007
Volume :
88
Database :
MEDLINE
Journal :
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
Publication Type :
Academic Journal
Accession number :
28142122
Full Text :
https://doi.org/10.1016/j.biopha.2017.01.046