VCC-1 over-expression inhibits cisplatin-induced apoptosis in HepG2 cells

Biochem Biophys Res Commun. 2012 Apr 6;420(2):336-42. doi: 10.1016/j.bbrc.2012.02.160. Epub 2012 Mar 7.

Abstract

Vascular endothelial growth factor-correlated chemokine 1 (VCC-1), a recently described chemokine, is hypothesized to be associated with carcinogenesis. However, the molecular mechanisms by which aberrant VCC-1 expression determines poor outcomes of cancers are unknown. In this study, we found that VCC-1 was highly expressed in hepatocellular carcinoma (HCC) tissue. It was also associated with proliferation of HepG2 cells, and inhibition of cisplatin-induced apoptosis of HepG2 cells. Conversely, down-regulation of VCC-1 in HepG2 cells increased cisplatin-induced apoptosis of HepG2 cells. In summary, these results suggest that VCC-1 is involved in cisplatin-induced apoptosis of HepG2 cells, and also provides some evidence for VCC-1 as a potential cellular target for chemotherapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / metabolism*
  • Carcinoma, Hepatocellular / pathology
  • Cell Line, Tumor
  • Cell Proliferation
  • Chemokines / genetics
  • Chemokines / metabolism*
  • Chemokines, CXC
  • Cisplatin / pharmacology*
  • Drug Resistance, Neoplasm*
  • Female
  • Gene Expression
  • Hep G2 Cells
  • Humans
  • Liver Neoplasms / genetics
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / pathology
  • Male
  • Middle Aged

Substances

  • Antineoplastic Agents
  • CXCL17 protein, human
  • Chemokines
  • Chemokines, CXC
  • Cisplatin