期刊
CELLS
卷 8, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/cells8111350
关键词
ER stress; autophagy; BAP31; STX17; tumor suppression; stress adaptation
类别
资金
- JSPS [16K18874]
- Takeda Science Foundation
- Uehara Memorial Foundation
- Astellas Foundation for Research on Metabolic Disorders
- Inamori Foundation
- Japan Prize Foundation
- Grants-in-Aid for Scientific Research [16K18874] Funding Source: KAKEN
Cancer cells modulate their metabolism to proliferate and survive under the metabolic stress condition, which is known as endoplasmic reticulum (ER) stress. Therefore, cancer cells should suppress ER stress-mediated cell death and induce autophagy-which recycles metabolites to provide energy and new macromolecules. In this study, we demonstrate that the ER membrane protein BAP31 acts to suppress adaptation to ER stress conditions, induce cell death, and suppress autophagy by forming a BAP31-STX17 protein complex. The loss of BAP31 stimulates tumor growth in metabolic stress conditions in vivo and enhances invasion activity. Therefore, BAP31 stimulates cell death and inhibits autophagy, and it can be considered a novel tumor suppressor factor that acts by preventing ER stress adaptation.
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