The CX3CL1/CX3CR1 reprograms glucose metabolism through HIF-1 pathway in pancreatic adenocarcinoma

J Cell Biochem. 2013 Nov;114(11):2603-11. doi: 10.1002/jcb.24608.

Abstract

One of the hallmarks of cancer is revised glucose metabolism that promotes cell survival and proliferation. In pancreatic cancer, the regulatory mechanism of glucose metabolism remains to be elucidated. In this study, we found that CX3CR1 is expressed in pancreatic cancer cells lines. Exogenous or transfected CX3CL1 increased glucose uptake and lactate secretion. CX3CL1 stimulated HIF-1 expression through PI3K/Akt and MAPK pathways. Furthermore, knockdown of HIF-1 blocked CX3CL1-modified glucose metabolism in pancreatic adenocarcinoma cells. In conclusion, the CX3CL1/CX3CR1 reprograms glucose metabolism through HIF-1 pathway in pancreatic cancer cells.

Keywords: CX3CL1; GLUCOSE METABOLISM; HYPOXIA-INDUCIBLE FACTOR-1; PANCREATIC ADENOCARCINOMA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CX3C Chemokine Receptor 1
  • Cell Line, Tumor
  • Chemokine CX3CL1 / genetics
  • Chemokine CX3CL1 / metabolism*
  • Gene Expression Regulation, Neoplastic / genetics
  • Gene Expression Regulation, Neoplastic / physiology
  • Glucose / metabolism*
  • HEK293 Cells
  • Humans
  • Hypoxia-Inducible Factor 1 / genetics
  • Hypoxia-Inducible Factor 1 / metabolism*
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / metabolism*
  • Receptors, Chemokine / genetics
  • Receptors, Chemokine / metabolism*

Substances

  • CX3C Chemokine Receptor 1
  • CX3CL1 protein, human
  • CX3CR1 protein, human
  • Chemokine CX3CL1
  • Hypoxia-Inducible Factor 1
  • Receptors, Chemokine
  • Glucose