ArticleCell cycle (Georgetown, Tex.)2018
P53 enhances apoptosis induced by doxorubicin only under conditions of severe DNA damage.
Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 55 citations in OpenAlex.
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- The impact of scaRNA12 deregulation on p53-mediated cellular stress response in B-cell precursor acute lymphoblastic leukaemia.British journal of haematology · 2026Article
- CMTM6/PD-L1-targeted AAV promotes anti-tumor immune responses and chemotherapy responsiveness.Frontiers in immunology · 2026Article
- Hepatoprotection by Methylene Blue Against Doxorubicin Toxicity Through Coordinated Modulation of Oxidative Stress, ER Stress, and Apoptotic Pathways.Pharmaceuticals (Basel, Switzerland) · 2025Article
- DDX3X/MAVS alleviates doxorubicin‑induced cardiotoxicity by regulating stress granules.Molecular medicine reports · 2025Article
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- Doxorubicin or Epirubicin Versus Liposomal Doxorubicin Therapy-Differences in Cardiotoxicity.Cardiovascular toxicology · 2025Review
- Small Extracellular Vesicles from Breast Cancer Cells Induce Cardiotoxicity.International journal of molecular sciences · 2025Article
- Unveiling the Protective Role of Metformin against Chemotherapy-induced Cardiotoxicity: A Comprehensive Scoping Review on Non-clinical Studies.Current medicinal chemistry · 2025Article
- Upregulation of YPEL3 expression and induction of human breast cancer cell death by microRNAs.Toxicological research · 2024Article
- Identification of new benzofuran derivatives as STING agonists with broad-spectrum antiviral activity.Virus research · 2024Article
- An MDM2 degrader shows potent cytotoxicity to MDM2-overexpressing acute lymphoblastic leukemia cells with minimal toxicity to normal cells/tissues.Cancer letters · 2024Article
- Suppression of the long non-coding RNA LINC01279 triggers autophagy and apoptosis in lung cancer by regulating FAK and SIN3A.Discover oncology · 2024Article
- In Vitro Anticancer Activity of Novel Ciprofloxacin Mannich Base in Lung Adenocarcinoma and High-Grade Serous Ovarian Cancer Cell Lines via Attenuating MAPK Signaling Pathway.Molecules (Basel, Switzerland) · 2023Article
- PKR-Mediated Phosphorylation of eIF2a and CHK1 Is Associated with Doxorubicin-Mediated Apoptosis in HCC1143 Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Nanoparticles design considerations to co-deliver nucleic acids and anti-cancer drugs for chemoresistance reversal.International journal of pharmaceutics: X · 2022Article
- Transgenic construction and functional miRNA analysis identify the role of miR-7 in prostate cancer suppression.Oncogene · 2022Article
- SIRT1 inhibition-induced senescence as a strategy to prevent prostate cancer progression.Molecular carcinogenesis · 2022Article
- Severe cellular stress drives apoptosis through a dual control mechanism independently of p53.Cell death discovery · 2022Review
- Compound cellular stress maximizes apoptosis independently of p53 in glioblastoma.Cell cycle (Georgetown, Tex.) · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously demonstrated that Bim is the main BH3-only protein replacing Bak/Bax from Bcl-xl to activate apoptosis in a p53-independent manner in response to doxorubicin in prostate cancer. However, the comparison of doxorubicin treatment between LNCaP cells carrying p53-wild type and PC3 cells carrying p53-null suggested that p53 might be essential for maximizing apoptosis. Inhibition of ATM did not affect doxorubicin-induced apoptosis. Overexpression of p53 did not affect ABT-263-induced apoptosis and nevertheless, the combination of doxorubicin with ABT-263 induced higher apoptotic responses than did doxorubicin or ABT-263 alone. These results advocated that doxorubicin-induced DNA damage controls p53 function for intensifying apoptosis. Indeed, overexpression of p53 only enhanced apoptosis under conditions of severe DNA damage induced by high concentrations of doxorubicin in LNCaP cells. Immunofluorescence staining showed vague γH2AX foci and enlarged nuclei in LNCaP cells in response to high concentrations of doxorubicin, en route to apoptosis. In addition, our results revealed that the apoptosis in response to DNA replication stress induced by CFS-1686, a catalytic inhibitor of topoisomerase, is p53-independent. Interestingly, the combination of doxorubicin with CFS-1686 generated DNA damage and replication stress simultaneously, resulting in a synergistic apoptotic effect in prostate cancer cells. Thus, we concluded that p53 is a sensor for enhanced apoptosis in response to DNA damage stress, not DNA replication stress, at least in prostate cancer.
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