ArticleScience advances2019
PP2Cδ inhibits p300-mediated p53 acetylation via ATM/BRCA1 pathway to impede DNA damage response in breast cancer.
Article in Science advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- The Landscape of BRCA1-Associated Post-Translational Modifications.Cell biology international · 2026Review
- Combined inhibition of PLK4 and PPM1D promotes cell death in cancer cells with 17q amplification.Cancer cell international · 2026Article
- Natural Products Targeting Acetylation in Bladder Cancer: Mechanistic Basis, Therapeutic Potential, and Future Perspectives.Current issues in molecular biology · 2026Review
- Lithospermic Acid Improves Doxorubicin-Induced Cardiomyopathy Through Sirtuin-3-Mediated Deacetylation of p53.Phytotherapy research : PTR · 2026Article
- Homoharringtonine and Gilteritinib Synergistically Induce Apoptosis and Suppress Viability in FLT3-ITD-Positive AML Cells.Biomedicines · 2026Article
- Smad1 Promotes Tumorigenicity and Chemoresistance of Glioblastoma by Sequestering p300 From p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- PPM1D activity promotes cellular transformation by preventing senescence and cell death.Oncogene · 2024Article
- Crosstalk between SUMOylation and other post-translational modifications in breast cancer.Cellular & molecular biology letters · 2024Review
- PPM1D activity promotes the replication stress caused by cyclin E1 overexpression.Molecular oncology · 2024Article
- α-Catenin acetylation is essential for its stability and blocks its tumor suppressor effects in breast cancer through Yap1.Cancer gene therapy · 2023Article
- GET4 is a novel driver gene in colorectal cancer that regulates the localization of BAG6, a nucleocytoplasmic shuttling protein.Cancer science · 2022Article
- Metabolite-derived protein modifications modulating oncogenic signaling.Frontiers in oncology · 2022Review
- ATR/ATM-Mediated Phosphorylation of BRCA1 T1394 Promotes Homologous Recombinational Repair and GCancer research · 2021Article
- Excision of mutagenic replication-blocking lesions suppresses cancer but promotes cytotoxicity and lethality in nitrosamine-exposed mice.Cell reports · 2021Article
- PP2Cδ Controls the Differentiation and Function of Dendritic Cells Through Regulating the NSD2/mTORC2/ACLY Pathway.Frontiers in immunology · 2021Article
- Licochalcone A is a Natural Selective Inhibitor of Arginine Methyltransferase 6.The Biochemical journal · 2020Article
- Anti‑proliferative effect of honokiol on SW620 cells through upregulating BMP7 expression via the TGF‑β1/p53 signaling pathway.Oncology reports · 2020Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Although nuclear type 2C protein phosphatase (PP2Cδ) has been demonstrated to be pro-oncogenic with an important role in tumorigenesis, the underlying mechanisms that link aberrant PP2Cδ levels with cancer development remain elusive. Here, we found that aberrant PP2Cδ activity decreases p53 acetylation and its transcriptional activity and suppresses doxorubicin-induced cell apoptosis. Mechanistically, we show that BRCA1 facilitates p300-mediated p53 acetylation by complexing with these two proteins and that S1423/1524 phosphorylation is indispensable for this regulatory process. PP2Cδ, via dephosphorylation of ATM, suppresses DNA damage-induced BRCA1 phosphorylation, leading to inhibition of p300-mediated p53 acetylation. Furthermore, PP2Cδ levels correlate with histological grade and are inversely associated with BRCA1 phosphorylation and p53 acetylation in breast cancer specimens. C23, our newly developed PP2Cδ inhibitor, promotes the anticancer effect of doxorubicin in MCF-7 xenograft-bearing nude mice. Together, our data indicate that PP2Cδ impairs p53 acetylation and DNA damage response by compromising BRCA1 function.
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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.