Modulation of endoplasmic reticulum (ER) stress-induced autophagy by C/EBP homologous protein (CHOP) and inositol-requiring enzyme 1α (IRE1α) in human colon cancer cells

Biochem Biophys Res Commun. 2014 Mar 7;445(2):524-33. doi: 10.1016/j.bbrc.2014.02.054. Epub 2014 Feb 21.

Abstract

To explore the relationship between UPR and autophagy in intestinal epithelial cells, we investigated whether autophagy was induced by endoplasmic reticulum (ER) stress in colon cancer cell lines. We demonstrated that autophagy was induced by ER stress in HT29, SW480, and Caco-2 cells. In these cells, inositol-requiring enzyme1α (IRE1α) and C/EBP homologous protein (CHOP) were involved in the ER stress-autophagy pathway, and CHOP was a regulator of IRE1α protein expression. Our findings suggest that CHOP promotes IRE1α and autophagy especially in ER stress conditions. This study will provide important insights into the disclosure of the ER stress-autophagy pathway.

Keywords: Autophagy; CHOP; ER stress; IRE1α.

MeSH terms

  • Autophagy*
  • Cell Line, Tumor
  • Colon / metabolism*
  • Colon / pathology
  • Colonic Neoplasms / genetics
  • Colonic Neoplasms / metabolism*
  • Colonic Neoplasms / pathology
  • Endoplasmic Reticulum Stress*
  • Endoribonucleases / genetics
  • Endoribonucleases / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Gene Knockdown Techniques
  • Humans
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Transcription Factor CHOP / genetics
  • Transcription Factor CHOP / metabolism*
  • Unfolded Protein Response

Substances

  • Transcription Factor CHOP
  • ERN1 protein, human
  • Protein Serine-Threonine Kinases
  • Endoribonucleases