BAP31 Inhibits Cell Adaptation to ER Stress Conditions, Negatively Regulating Autophagy Induction by Interaction with STX17

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.