RRC ID 58136
Author Machihara K, Namba T.
Title BAP31 Inhibits Cell Adaptation to ER Stress Conditions, Negatively Regulating Autophagy Induction by Interaction with STX17.
Journal Cells
Abstract 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.
Volume 8(11)
Published 2019-10-30
DOI 10.3390/cells8111350
PII cells8111350
PMID 31671609
PMC PMC6912744
MeSH Adaptor Proteins, Vesicular Transport / genetics Adaptor Proteins, Vesicular Transport / metabolism Animals Apoptosis Autophagy* Autophagy-Related Proteins / genetics Autophagy-Related Proteins / metabolism Biomarkers, Tumor / genetics Biomarkers, Tumor / metabolism Bone Neoplasms / genetics Bone Neoplasms / metabolism Bone Neoplasms / pathology* Endoplasmic Reticulum / metabolism* Endoplasmic Reticulum Stress* Gene Expression Regulation, Neoplastic Humans Male Membrane Proteins / genetics Membrane Proteins / metabolism* Mice Mice, Inbred BALB C Mice, Nude Osteosarcoma / genetics Osteosarcoma / metabolism Osteosarcoma / pathology* Qa-SNARE Proteins / genetics Qa-SNARE Proteins / metabolism* Tumor Cells, Cultured Xenograft Model Antitumor Assays
IF 5.656
Times Cited 0
Human and Animal Cells NB1RGB(RCB0222)