Division of Gastroenterology, Tohoku University Graduate School of Medicine, Miyagi, Japan.
Department of Gastroenterology, Iwaki-Kyoritsu General Hospital, Fukushima, Japan.
Biochem Biophys Res Commun. 2014 Mar 7;445(2):524-33. doi: 10.1016/j.bbrc.2014.02.054. Epub 2014 Feb 21.
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.
为了探究未折叠蛋白反应(UPR)与肠上皮细胞自噬之间的关系,我们研究了内质网(ER)应激是否会诱导结肠癌细胞系发生自噬。我们证明,内质网应激会诱导 HT29、SW480 和 Caco-2 细胞发生自噬。在这些细胞中,肌醇需求酶 1α(IRE1α)和 C/EBP 同源蛋白(CHOP)参与了 ER 应激-自噬途径,而 CHOP 是 IRE1α 蛋白表达的调节剂。我们的研究结果表明,CHOP 促进了 IRE1α 和自噬,尤其是在 ER 应激条件下。本研究将为揭示 ER 应激-自噬途径提供重要的见解。