ArticleEndocrine-related cancer2020
p300 is upregulated by docetaxel and is a target in chemoresistant prostate cancer.
Article in Endocrine-related cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- CBP/p300, a promising therapeutic target for prostate cancer.Journal of translational medicine · 2025Review
- Evolving roles for the androgen receptor and its protein interactome in castration-resistant prostate cancer.Oncogene · 2025Review
- Androgen Receptor Signalling in Prostate Cancer: Mechanisms of Resistance to Endocrine Therapies.Research and reports in urology · 2025Review
- Genetic dysregulation of EP300 in cancers in light of cancer epigenome control - targeting of p300-proficient and -deficient cancers.Molecular therapy. Oncology · 2024Review
- Article
- AR coactivators, CBP/p300, are critical mediators of DNA repair in prostate cancer.bioRxiv : the preprint server for biology · 2024Article
- Androgen Receptor-Interacting Proteins in Prostate Cancer Development and Therapy Resistance.The American journal of pathology · 2024Review
- Loss of SYNCRIP unleashes APOBEC-driven mutagenesis, tumor heterogeneity, and AR-targeted therapy resistance in prostate cancer.Cancer cell · 2023Article
- Unravelling the Role of P300 and TMPRSS2 in Prostate Cancer: A Literature Review.International journal of molecular sciences · 2023Review
- The Role of Histone Modification in DNA Replication-Coupled Nucleosome Assembly and Cancer.International journal of molecular sciences · 2023Review
- Review
- Post-Translational Modifications by Lipid Metabolites during the DNA Damage Response and Their Role in Cancer.Biomolecules · 2022Review
- Activation ofCancers · 2022Article
- Somatic Alterations Impact AR Transcriptional Activity and Efficacy of AR-Targeting Therapies in Prostate Cancer.Cancers · 2021Review
- Review
- MYC-Mediated Ribosomal Gene Expression Sensitizes Enzalutamide-resistant Prostate Cancer Cells to EP300/CREBBP Inhibitors.The American journal of pathology · 2021Article
- Targeting the p300/CBP Axis in Lethal Prostate Cancer.Cancer discovery · 2021Article
- Integrated Analysis to Study the Relationship between Tumor-Associated Selenoproteins: Focus on Prostate Cancer.International journal of molecular sciences · 2020Article
- The Role of p300 and TMPRSS2 in Prostate Cancer: Immunohistochemical Perspectives and Gleason Correlations.Cancer diagnosis & prognosisArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
Abstract
Administration of the microtubule inhibitor docetaxel is a common treatment for metastatic castration-resistant prostate cancer (mCRPC) and results in prolonged patient overall survival. Usually, after a short period of time chemotherapy resistance emerges and there is urgent need to find new therapeutic targets to overcome therapy resistance. The lysine-acetyltransferase p300 has been correlated to prostate cancer (PCa) progression. Here, we aimed to clarify a possible function of p300 in chemotherapy resistance and verify p300 as a target in chemoresistant PCa. Immunohistochemistry staining of tissue samples revealed significantly higher p300 protein expression in patients who received docetaxel as a neoadjuvant therapy compared to control patients. Elevated p300 expression was confirmed by analysis of publicly available patient data, where significantly higher p300 mRNA expression was found in tissue of mCRPC tumors of docetaxel-treated patients. Consistently, docetaxel-resistant PCa cells showed increased p300 protein expression compared to docetaxel-sensitive counterparts. Docetaxel treatment of PCa cells for 72 h resulted in elevated p300 expression. shRNA-mediated p300 knockdown did not alter colony formation efficiency in docetaxel-sensitive cells, but significantly reduced clonogenic potential of docetaxel-resistant cells. Downregulation of p300 in docetaxel-resistant cells also impaired cell migration and invasion. Taken together, we showed that p300 is upregulated by docetaxel, and our findings suggest that p300 is a possible co-target in treatment of chemoresistant PCa.
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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.