ArticleOncogene2004
Inhibition of p53 function diminishes androgen receptor-mediated signaling in prostate cancer cell lines.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 94 citations in OpenAlex.
- MDM2 and Ki-67 predict for distant metastasis and mortality in men treated with radiotherapy and androgen deprivation for prostate cancer: RTOG 92-02.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009Trial
- Genomic biomarkers of survival in patients with metastatic hormone-sensitive prostate cancer undergoing intensified androgen deprivation therapy.Prostate cancer and prostatic diseases · 2025Article
- Integrating Aggressive-Variant Prostate Cancer-Associated Tumor Suppressor Gene Status with Clinical Variables to Refine Prognosis and Predict Androgen Receptor Pathway Inhibitor Response in Metastatic Hormone-Sensitive Setting.International journal of molecular sciences · 2025Article
- The Emerging Predictive and Prognostic Role of Aggressive-Variant-Associated Tumor Suppressor Genes Across Prostate Cancer Stages.International journal of molecular sciences · 2025Review
- Interactions between key genes and pathways in prostate cancer progression and therapy resistance.Frontiers in oncology · 2025Review
- Increased Local Testosterone Levels Alter Human Fallopian Tube mRNA Profile and Signaling.Cancers · 2023Article
- Second generation androgen receptor antagonist, TQB3720 abrogates prostate cancer growthFrontiers in pharmacology · 2023Article
- Regulatory Role of Fatty Acid Metabolism-Related Long Noncoding RNA in Prostate Cancer: A Computational Biology Study Analysis.Journal of oncology · 2023Article
- Article
- Novel MDM2 Inhibitor XR-2 Exerts Potent Anti-Tumor Efficacy and Overcomes Enzalutamide Resistance in Prostate Cancer.Frontiers in pharmacology · 2022Article
- TAF1A and ZBTB41 serve as novel key genes in cervical cancer identified by integrated approaches.Cancer gene therapy · 2021Article
- Article
- Review
- Metabolic reprogramming as an emerging mechanism of resistance to endocrine therapies in prostate cancer.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- The Interplay Between Prostate Cancer Genomics, Metabolism, and the Epigenome: Perspectives and Future Prospects.Frontiers in oncology · 2021Review
- Linalool inhibits 22Rv1 prostate cancer cell proliferation and induces apoptosis.Oncology letters · 2020Article
- Constitutively active androgen receptor supports the metastatic phenotype of endocrine-resistant hormone receptor-positive breast cancer.Cell communication and signaling : CCS · 2020Article
- Anticancer Imidazoacridinone C-1311 is Effective in Androgen-Dependent and Androgen-Independent Prostate Cancer Cells.Biomedicines · 2020Article
- Prevention of Prostate Cancer in Transgenic Adenocarcinoma of the Mouse Prostate Mice by Yellow Passion Fruit Extract and Antiproliferative Effects of Its Bioactive Compound Piceatannol.Journal of cancer prevention · 2020Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current therapy for advanced prostate cancer is mainly based on androgen deprivation, although most patients relapse to androgen-insensitive disease. Several mechanisms contributing to androgen-independent growth including alterations in the structure or expression of the androgen receptor (AR) and its cofactors have been identified. Recent evidence suggests that p53 is involved in androgen signaling. The analysis of the effect of p53 on androgen signaling was performed in 22Rv1 and LNCaP prostate cancer cells that express both p53 and AR. The overexpression of p53 diminished the androgenic response in both cell lines in a reporter gene assay. Conversely, the inhibition of p53 by three different p53 inhibitors, Pifithrin-1alpha (PFT-1alpha), an inhibitor of p53-dependent transactivation; MDM2, a regulator of p53 expression; and a dominant-negative N-terminally truncated p53 gene also reduced transactivation of androgen-dependent reporter genes. The inactivation of p53 by PFT-1alpha decreased AR-protein expression in both 22Rv1 and LNCaP cells. Our findings confirm that the overexpression of wild-type p53 decreases androgen function, whereas p53 expression at physiological levels stabilizes AR signaling. Thus, our findings suggest that there is a balance of AR and p53 expression during the androgen-dependent growth of prostate cancer, which is obliterated during further progression of the disease.
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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.