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.

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.

• Authors: Yosuke Shimodaira, Seiichi Takahashi, Yoshitaka Kinouchi, Katsuya Endo, Hisashi Shiga, Yoichi Kakuta, Masatake Kuroha, Tooru Shimosegawa
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 445 Issue 2 Pg. 524-33 (Mar 07 2014) ISSN: 1090-2104 [Electronic] United States
• PMID: 24565834 (Publication Type: Journal Article)
• Copyright: Copyright © 2014 Elsevier Inc. All rights reserved.

Chemical References

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

Topics

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