ArticleMolecular oncology2021
Mechanistic insights into p53-regulated cytotoxicity of combined entinostat and irinotecan against colorectal cancer cells.
Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
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- Targeting epigenetic modifications as an emerging immunotherapeutic strategy for cancers.Immunologic research · 2025Review
- Genistein potentiated the cytotoxic effect of entinostat in colorectal cancer cell lines.Research in pharmaceutical sciences · 2025Article
- 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
- DNA damage response regulator ATR licenses PINK1-mediated mitophagy.Nucleic acids research · 2025Article
- DNA Damage-Induced Ferroptosis: A Boolean Model Regulating p53 and Non-Coding RNAs in Drug Resistance.Proteomes · 2025Article
- Synergy of retinoic acid and BH3 mimetics in MYC(N)-driven embryonal nervous system tumours.British journal of cancer · 2024Article
- Novel hydroxamic acid derivative induces apoptosis and constrains autophagy in leukemic cells.Journal of advanced research · 2024Article
- Understanding Cancer's Defense against Topoisomerase-Active Drugs: A Comprehensive Review.Cancers · 2024Review
- Article
- Global metabolic alterations in colorectal cancer cells during irinotecan-induced DNA replication stress.Cancer & metabolism · 2022Article
- Inhibitors of class I HDACs and of FLT3 combine synergistically against leukemia cells with mutant FLT3.Archives of toxicology · 2022Article
- The Class I HDAC Inhibitor, MS-275, Prevents Oxaliplatin-Induced Chronic Neuropathy and Potentiates Its Antiproliferative Activity in Mice.International journal of molecular sciences · 2021Article
- The HROC-Xenobank-A High Quality Assured PDX Biobank of >100 Individual Colorectal Cancer Models.Cancers · 2021Article
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Authors and funding
21 authors at 7 institutions in 3 countries.
Funding
Abstract
Late-stage colorectal cancer (CRC) is still a clinically challenging problem. The activity of the tumor suppressor p53 is regulated via post-translational modifications (PTMs). While the relevance of p53 C-terminal acetylation for transcriptional regulation is well defined, it is unknown whether this PTM controls mitochondrially mediated apoptosis directly. We used wild-type p53 or p53-negative human CRC cells, cells with acetylation-defective p53, transformation assays, CRC organoids, and xenograft mouse models to assess how p53 acetylation determines cellular stress responses. The topoisomerase-1 inhibitor irinotecan induces acetylation of several lysine residues within p53. Inhibition of histone deacetylases (HDACs) with the class I HDAC inhibitor entinostat synergistically triggers mitochondrial damage and apoptosis in irinotecan-treated p53-positive CRC cells. This specifically relies on the C-terminal acetylation of p53 by CREB-binding protein/p300 and the presence of C-terminally acetylated p53 in complex with the proapoptotic BCL2 antagonist/killer protein. This control of C-terminal acetylation by HDACs can mechanistically explain why combinations of irinotecan and entinostat represent clinically tractable agents for the therapy of p53-proficient CRC.
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