ArticleProceedings of the National Academy of Sciences of the United States of America2010
p53-dependent regulation of autophagy protein LC3 supports cancer cell survival under prolonged starvation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.
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Who cites it
143 citing papers in PubMed, 231 citations in OpenAlex.
- Transcriptional and epigenetic regulation of autophagy: mechanisms, disease relevance and therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- The guardian of the genome meets immunotherapy: p53-based strategies.Frontiers in immunology · 2026Review
- Polysialylation of Glioblastoma Cells Is Regulated by Autophagy Under Nutrient Deprivation.International journal of molecular sciences · 2025Article
- Isowalsuranolide targets TrxR1/2 and triggers lysosomal biogenesis and autophagy via the p53-TFEB/TFE3 axis.Science China. Life sciences · 2025Article
- Article
- Side-stepping the guardian of the genome: current cancer therapeutics targeting mutant p53.Frontiers in pharmacology · 2025Review
- Targeting Molecular Pathways in Breast Cancer Using Plant-Derived Bioactive Compounds: A Comprehensive Review.Journal of experimental pharmacology · 2025Review
- The Estrogen-Autophagy Axis: Insights into Cytoprotection and Therapeutic Potential in Cancer and Infection.International journal of molecular sciences · 2024Review
- Chemically programmed metabolism drives a superior cell fitness for cartilage regeneration.Science advances · 2024Article
- Mitochondrial damage and impaired mitophagy contribute to disease progression in SCA6.Acta neuropathologica · 2024Article
- Role of SIRT1 in Chemoresistant Leukemia.International journal of molecular sciences · 2023Review
- A Deadly Liaison between Oxidative Injury and p53 Drives Methyl-Gallate-Induced Autophagy and Apoptosis in HCT116 Colon Cancer Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Hypoxia Changes Energy Metabolism and Growth Rate in Non-Small Cell Lung Cancer Cells.Cancers · 2023Article
- UHMK1 promotes lung adenocarcinoma oncogenesis by regulating the PI3K/AKT/mTOR signaling pathway.Thoracic cancer · 2023Article
- Autophagic reprogramming of bone marrow-derived macrophages.Immunologic research · 2023Article
- Tissue specificity and spatio-temporal dynamics of the p53 transcriptional program.Cell death and differentiation · 2023Review
- Acetylcholine facilitates localized synaptic potentiation and location specific feature binding.Frontiers in neural circuits · 2023Article
- Autophagy and Its Lineage-Specific Roles in the Hematopoietic System.Oxidative medicine and cellular longevity · 2023Review
- The complexity of p53-mediated metabolic regulation in tumor suppression.Seminars in cancer biology · 2022Review
83 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The p53 tumor suppressor is mutated in a high percentage of human tumors. However, many other tumors retain wild-type (wt) p53 expression, raising the intriguing possibility that they actually benefit from it. Recent studies imply a role for p53 in regulation of autophagy, a catabolic pathway by which eukaryotic cells degrade and recycle macromolecules and organelles, particularly under conditions of nutrient deprivation. Here, we show that, in many cell types, p53 confers increased survival in the face of chronic starvation. We implicate regulation of autophagy in this effect. In HCT116 human colorectal cancer cells exposed to prolonged nutrient deprivation, the endogenous wt p53 posttranscriptionally down-regulates LC3, a pivotal component of the autophagic machinery. This enables reduced, yet sustainable autophagic flux. Loss of p53 impairs autophagic flux and causes excessive LC3 accumulation upon starvation, culminating in apoptosis. Thus, p53 increases cell fitness by maintaining better autophagic homeostasis, adjusting the rate of autophagy to changing circumstances. We propose that some cancer cells retain wt p53 to benefit from the resultant increased fitness under limited nutrient supply.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.