ArticleJournal of cellular and molecular medicine2014
Beclin-1-p53 interaction is crucial for cell fate determination in embryonal carcinoma cells.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- The Biological Role and Clinical Significance of BECLIN-1 in Cancer.International journal of molecular sciences · 2025Review
- Decoding the dual role of autophagy in cancer through transcriptional and epigenetic regulation.FEBS letters · 2025Review
- An overview of autophagy inhibition as a potential clinical strategy in cancer therapy.Molecular pharmacology · 2025Review
- Deciphering the dual role of autophagy in gastric cancer and gastroesophageal junction cancer: from tumor suppression to cancer progression.Discover oncology · 2025Review
- Mechanism of Drug Resistance to First-Line Chemotherapeutics Mediated by TXNDC17 in Neuroblastomas.Cancer reports (Hoboken, N.J.) · 2024Article
- Dissecting the multifaceted roles of autophagy in cancer initiation, growth, and metastasis: from molecular mechanisms to therapeutic applications.Medical oncology (Northwood, London, England) · 2024Review
- Transcriptional regulation of autophagy and its implications in human disease.Cell death and differentiation · 2023Review
- USP5-Beclin 1 axis overrides p53-dependent senescence and drives Kras-induced tumorigenicity.Nature communications · 2022Article
- ONX-0914 Induces Apoptosis and Autophagy with p53 Regulation in Human Glioblastoma Cells.Cancers · 2022Article
- Isolation, Characterization, and Autophagy Function of BECN1-Splicing Isoforms in Cancer Cells.Biomolecules · 2022Article
- Is Autophagy Always a Barrier to Cisplatin Therapy?Biomolecules · 2022Review
- p53 Modulation of Autophagy Signaling in Cancer Therapies: Perspectives Mechanism and Therapeutic Targets.Frontiers in cell and developmental biology · 2022Review
- Programmed cell death, redox imbalance, and cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2021Review
- Dying to Survive-The p53 Paradox.Cancers · 2021Review
- p53 Deacetylation Alleviates Sepsis-Induced Acute Kidney Injury by Promoting Autophagy.Frontiers in immunology · 2021Article
- Dual Roles of Autophagy and Their Potential Drugs for Improving Cancer Therapeutics.Biomolecules & therapeutics · 2020Review
- Influence of nonprotective autophagy and the autophagic switch on sensitivity to cisplatin in non-small cell lung cancer cells.Biochemical pharmacology · 2020Article
- The Inhibitory Effect of 6-Gingerol on Ubiquitin-Specific Peptidase 14 Enhances Autophagy-Dependent Ferroptosis and Anti-TumorFrontiers in pharmacology · 2020Article
- Mutant p53 as a Regulator and Target of Autophagy.Frontiers in oncology · 2020Review
- p53 at the Crossroads between Different Types of HDAC Inhibitor-Mediated Cancer Cell Death.International journal of molecular sciences · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging interest on the interrelationship between the apoptotic and autophagy pathways in the context of cancer chemotherapy is providing exciting discoveries. Complexes formed between molecules from both pathways present potential targets for chemotherapeutics design as disruption of such complexes could alter cell survival. This study demonstrates an important role of Beclin-1 and p53 interaction in cell fate decision of human embryonal carcinoma cells. The findings provide evidence for p53 interaction with Beclin-1 through the BH3 domain of the latter. This interaction facilitated Beclin-1 ubiquitination through lysine 48 linkage, resulting in proteasome-mediated degradation, consequently maintaining a certain constitutive level of Beclin-1. Disruption of Beclin-1-p53 interaction through shRNA-mediated down-regulation of p53 reduced Beclin-1 ubiquitination suggesting requirement of p53 for the process. Reduction of ubiquitination consequently resulted in an increase in Beclin-1 levels with cells showing high autophagic activity. Enforced overexpression of p53 in the p53 down-regulated cells restored ubiquitination of Beclin-1 reducing its level and lowering autophagic activity. The Beclin-1-p53 interaction was also disrupted by exposure to cisplatin-induced stress resulting in higher level of Beclin-1 because of lesser ubiquitination. This higher concentration of Beclin-1 increased autophagy and offered protection to the cells from cisplatin-induced death. Inhibition of autophagy by either pharmacological or genetic means during cisplatin exposure increased apoptotic death in vitro as well as in xenograft tumours grown in vivo confirming the protective nature of autophagy. Therefore, Beclin-1-p53 interaction defines one additional molecular subroutine crucial for cell fate decisions in embryonal carcinoma cells.
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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.