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Updated: Feb 27, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
CXCL10 accelerates EMT and metastasis by MMP-2 in hepatocellular carcinoma
Tingting Ren1, Lili Zhu2, Mingliang Cheng3
1Department of Biochemistry, Affiliated Hospital of Guiyang Medical College28 Guiyi Street, Guiyang 550004, Guizhou, China.
Abstract:
Human malignant hepatocellular carcinoma (HCC) is a common tumor, which severely threatens human health and shortens longevity. The poor prognosis of HCC is primarily attributed to distant metastases. C-X-C motif chemokine 10 (CXCL10) regulates the control of several cellular and developmental processes including tumor cell proliferation, apoptosis, and cell metastasis. Previous studies have confirmed that CXCL10 functions as an oncogene in several cancers. However, the expression and biological functions of CXCL10 in HCC, especially with regard to metastasis, need further investigation. In this study, CXCL10 was found to be over expressed in invasive HCC cells and HCC clinical samples. While the over-expression of CXCL10 enhanced migration, invasion, and metastasis of HCC cells in vitro as well as in vivo, silencing of CXCL10 resulted in inhibition of HCC cell metastasis. Further, CXCL10 was found to accelerate epithelial-mesenchymal transition of HCC cells. The microarray analysis indicated that matrix metallopeptidase-2 (MMP-2) functions as a downstream factor of CXCL10. This study demonstrates that CXCL10 partakes in the metastasis of HCC by activating MMP-2 expression.
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