ArticleCells2023
Quadra-Stable Dynamics of p53 and PTEN in the DNA Damage Response.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- The crosslink between autophagy and ferroptosis in polycystic ovary syndrome: from synergistic pathogenesis to targeted therapy.Journal of ovarian research · 2026Review
- Exosomes-Transferred lncRNA H19 Reverses Osimertinib Resistance by Upregulating PTEN via Sponging miR-148-3p in Non-Small Cell Lung Cancer.Oncology research · 2026Article
- Targeting NSCLC drug resistance: Systems biology insights into the MALAT1/miR-145-5p axis and Wip1 in regulating ferroptosis and apoptosis.Journal of the Royal Society, Interface · 2025Article
- Divergent PTEN-p53 interaction upon DNA damage in a human thyroid organoid model with germline PTEN mutations.Endocrine-related cancer · 2025Article
- The interplay between DNA damage response and mitochondrial dysfunction in radiotherapy.Frontiers in oncology · 2025Review
- PTEN-mediated senescence of lung epithelial cells drives ventilator-induced pulmonary fibrosis.Theranostics · 2025Article
- LncRNA PTENP1/miR-21/PTEN Axis Modulates EMT and Drug Resistance in Cancer: Dynamic Boolean Modeling for Cell Fates in DNA Damage Response.International journal of molecular sciences · 2024Article
- PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024Review
- A dynamic Boolean network reveals that the BMI1 and MALAT1 axis is associated with drug resistance by limiting miR-145-5p in non-small cell lung cancer.Non-coding RNA research · 2024Article
- The lncRNA DLX6-AS1/miR-16-5p axis regulates autophagy and apoptosis in non-small cell lung cancer: A Boolean model of cell death.Non-coding RNA research · 2023Article
- Oncogene-Induced Senescence Is a Crucial Antitumor Defense Mechanism of Human Endometrial Stromal Cells.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell fate determination is a complex process that is frequently described as cells traveling on rugged pathways, beginning with DNA damage response (DDR). Tumor protein p53 (p53) and phosphatase and tensin homolog (PTEN) are two critical players in this process. Although both of these proteins are known to be key cell fate regulators, the exact mechanism by which they collaborate in the DDR remains unknown. Thus, we propose a dynamic Boolean network. Our model incorporates experimental data obtained from NSCLC cells and is the first of its kind. Our network's wild-type system shows that DDR activates the G2/M checkpoint, and this triggers a cascade of events, involving p53 and PTEN, that ultimately lead to the four potential phenotypes: cell cycle arrest, senescence, autophagy, and apoptosis (quadra-stable dynamics). The network predictions correspond with the gain-and-loss of function investigations in the additional two cell lines (HeLa and MCF-7). Our findings imply that p53 and PTEN act as molecular switches that activate or deactivate specific pathways to govern cell fate decisions. Thus, our network facilitates the direct investigation of quadruplicate cell fate decisions in DDR. Therefore, we concluded that concurrently controlling PTEN and p53 dynamics may be a viable strategy for enhancing clinical outcomes.
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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.