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Updated: Oct 19, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
P53-regulated autophagy and its impact on drug resistance and cell fate
Daeun Shim1, Lei Duan1, Carl G Maki1
1Department of Cell and Molecular Medicine, Rush University Medical Center, Chicago, IL 60612, USA.
Abstract:
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.
Insights
The tumor suppressor p53 influences autophagy, a cellular recycling process. Modulating autophagy can enhance p53
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Wild-type p53 functions as a tumor suppressor by halting cancer cell growth via apoptosis or proliferation arrest.
- Autophagy is a cellular degradation and recycling process crucial for stress response and survival.
- The p53 protein's role in autophagy is context-dependent, influenced by its location, mutation status, and stress levels.
Purpose of the Study:
- To investigate the intricate relationship between p53 and autophagy in cancer.
- To explore how autophagy modulation impacts p53-mediated tumor suppression.
Main Methods:
- Literature review and analysis of existing studies on p53 and autophagy.
- Examination of experimental data linking p53 activity, autophagy flux, and cell fate.
Main Results:
- P53 can either promote or inhibit autophagy based on cellular context.
- Inhibition of autophagy has been shown to potentiate p53-induced apoptosis in cancer cells.
Conclusions:
- Autophagy plays a significant role in determining cell fate when p53 is activated.
- Targeting autophagy presents a potential strategy to augment p53-driven tumor suppression.
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