ArticleCell cycle (Georgetown, Tex.)2012
p53 expression controls prostate cancer sensitivity to chemotherapy and the MDM2 inhibitor Nutlin-3.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 110 citations in OpenAlex.
- Metabolic Modulation by Dimethyl Fumarate Alters Docetaxel Responses in Prostate Cancer Cells.International journal of molecular sciences · 2026Article
- Article
- Unveiling the Anticancer Potential of Verbascum aydogdui: Isolation, Characterization, and In Vitro Studies.Chemistry & biodiversity · 2026Article
- Functional and genomic characterization of LCN2-deficient PC-3 cells reveals insights into prostate cancer progression.Frontiers in molecular biosciences · 2026Article
- Unveiling oncogene-induced senescence: a new frontier in prostate cancer prognosis and therapy.Discover oncology · 2025Article
- CanPharmaceuticals (Basel, Switzerland) · 2025Review
- Depletion of TP53 in Human Pluripotent Stem Cells Triggers Malignant-Like Behavior.Advanced biology · 2025Article
- Exploring druggable targets and inflammation-mediated pathways in cancer: a Mendelian randomization analysis integrating transcriptomic and proteomic data.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Effect of Diosgenin in Suppressing Viability and Promoting Apoptosis of Human Prostate Cancer Cells: An Interplay with the G Protein-Coupled Oestrogen Receptor?International journal of molecular sciences · 2024Article
- Neuroendocrine Prostate Cancer Drivers SOX2 and BRN2 Confer Differential Responses to Imipridones ONC201, ONC206, and ONC212 in Prostate Cancer Cell Lines.bioRxiv : the preprint server for biology · 2024Article
- TRIM47 silencing inhibits the malignant biological behaviors of prostate cancer cells by regulating MDM2/p53 signaling.Cell biochemistry and biophysics · 2024Article
- P53 together with ferroptosis: a promising strategy leaving cancer cells without escape.Acta biochimica et biophysica Sinica · 2024Article
- Self-Assembled Molecular Complexes of 1,10-Phenanthroline and 2-Aminobenzimidazoles: Synthesis, Structure Investigations, and Cytotoxic Properties.Molecules (Basel, Switzerland) · 2024Article
- Neuroendocrine prostate cancer drivers SOX2 and BRN2 confer differential responses to imipridones ONC201, ONC206, and ONC212 in prostate cancer cell lines.American journal of translational research · 2024Article
- The CDK7 inhibitor CT7001 (Samuraciclib) targets proliferation pathways to inhibit advanced prostate cancer.British journal of cancer · 2023Article
- DDX5 mRNA-targeting antisense oligonucleotide as a new promising therapeutic in combating castration-resistant prostate cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- CRISPR screens reveal genetic determinants of PARP inhibitor sensitivity and resistance in prostate cancer.Nature communications · 2023Article
- Biological Response of Human Cancer Cells to Ionizing Radiation in Combination with Gold Nanoparticles.Cancers · 2022Article
- Silibinin Radiosensitizes EGF Receptor-knockdown Prostate Cancer Cells by Attenuating DNA Repair Pathways.Journal of cancer prevention · 2022Article
- S-Adenosylmethionine affects ERK1/2 and STAT3 pathway in androgen-independent prostate cancer cells.Molecular biology reports · 2022Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is the second most commonly diagnosed cancer in men, and approximately one-third of those diagnosed succumb to the disease. The development of prostate cancer from small regions of hyperplasia to invasive tumors requires genetic and epigenetic alterations of critical cellular components to aid in the development of cells more adapted for aberrant growth. The p53 transcription factor is a critical element in the cell's ability to regulate the cell cycle and its response to DNA damage. Mutations within the DNA-binding domain of p53 are common and allow the formation of tetramers; however, these alterations prevent this protein complex from associating with target gene promoters. In the present study, we examined the effects of p53 functionality in prostate cancer cells that harbored wild-type (WT) or mutant forms of the protein in response to commonly used chemotherapeutic drugs. The androgen receptor positive 22Rv-1 and LNCaP prostate cancer cell lines carry WT p53 and were demonstrated to have a decrease in chemotherapeutic drug sensitivity when transfected with a dominant-negative (DN) p53. Conversely, expression of the WT p53 in the p53-mutated and more advanced DU145 prostate cancer cell line significantly increased its overall sensitivity to anti-neoplastic drugs. Furthermore, analysis of colony formation in soft agar revealed that the functional status of p53 in each cell line altered the cell's ability to proliferate in an anchorage-independent fashion. Prostate cancer colony growth was more prevalent when p53 transcriptional activity was decreased, whereas growth was more limited in the presence of functional p53. These results demonstrate that the functional status of the tumor suppressor p53 is important in the progression of prostate cancer and dictates the overall effectiveness a given drug would have on disease treatment.
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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.