P53-regulated autophagy and its impact on drug resistance and cell fate

• Published in: Cancer drug resistance Vol. 4; no. 1; pp. 85 - 95
• Main Authors: Shim, Daeun, Duan, Lei, Maki, Carl G
• Format: Journal Article
• Language: English
• Published: OAE Publishing Inc 01.01.2021
• Subjects: Review
• ISSN: 2578-532X
• DOI: 10.20517/cdr.2020.85

Wild-type p53 is a stress-responsive transcription factor and a potent tumor suppressor. P53 inhibits the growth of incipient cancer cells by blocking their proliferation or inducing their death through apoptosis. Autophagy is a self-eating process that plays a key role in response to stress. During autophagy, organelles and other intracellular components are degraded in autophagolysosomes and the autophagic breakdown products are recycled into metabolic and energy producing pathways needed for survival. P53 can promote or inhibit autophagy depending on its subcellular localization, mutation status, and the level of stress. Blocking autophagy has been reported in several studies to increase p53-mediated apoptosis, revealing that autophagy can influence cell-fate in response to activated p53 and is a potential target to increase p53-dependent tumor suppression.