ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012
PTEN deletion in prostate cancer cells does not associate with loss of RAD51 function: implications for radiotherapy and chemotherapy.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 82 papers.
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82 citing papers in PubMed, 129 citations in OpenAlex.
- CD73 inhibition overcomes adaptive immune resistance to PARP inhibition in models of prostate cancer.The Journal of clinical investigation · 2026Article
- PTEN deficiency confers sensitivity to ATR inhibitor-based treatment in high-grade serous ovarian cancer.The Journal of clinical investigation · 2026Article
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- Dual PARP/Tankyrase Inhibition Enhances Antitumor Efficacy in PTEN-Deficient Endometrial Cancer.Journal of cellular and molecular medicine · 2026Article
- Integrated Phenotypic and Transcriptomic Profiling Positions ONC212 as a Lead Imipridone in Androgen-Independent Prostate Cancer Models.International journal of molecular sciences · 2026Article
- Functional and genomic characterization of LCN2-deficient PC-3 cells reveals insights into prostate cancer progression.Frontiers in molecular biosciences · 2026Article
- The Emerging Predictive and Prognostic Role of Aggressive-Variant-Associated Tumor Suppressor Genes Across Prostate Cancer Stages.International journal of molecular sciences · 2025Review
- Long-term zinc treatment alters the mechanical properties and metabolism of prostate cancer cells.Cancer cell international · 2024Article
- Dual targeting of the androgen receptor and PI3K/AKT/mTOR pathways in prostate cancer models improves antitumor efficacy and promotes cell apoptosis.Molecular oncology · 2024Article
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- Uncovering the Secrets of Prostate Cancer's Radiotherapy Resistance: Advances in Mechanism Research.Biomedicines · 2023Review
- PTEN Loss Enhances Error-Prone DSB Processing and Tumor Cell Radiosensitivity by Suppressing RAD51 Expression and Homologous Recombination.International journal of molecular sciences · 2022Article
- Prostate Cancer Review: Genetics, Diagnosis, Treatment Options, and Alternative Approaches.Molecules (Basel, Switzerland) · 2022Review
- Precision Medicine forCancers · 2022Review
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- Response prediction biomarkers and drug combinations of PARP inhibitors in prostate cancer.Acta pharmacologica Sinica · 2021Review
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- Perspectives on PARP Inhibitor Combinations for Ovarian Cancer.Frontiers in oncology · 2021Review
- ATM Kinase Inhibition Preferentially Sensitises PTEN-Deficient Prostate Tumour Cells to Ionising Radiation.Cancers · 2020Article
- Frequency and prognostic value of mutations associated with the homologous recombination DNA repair pathway in a large pan cancer cohort.Scientific reports · 2020Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
purposePTEN deletions in prostate cancer are associated with tumor aggression and poor outcome. Recent studies have implicated PTEN as a determinant of homologous recombination (HR) through defective RAD51 function. Similar to BRCA1/2-defective tumor cells, PTEN-null prostate and other cancer cells have been reported to be sensitive to PARP inhibitors (PARPi). To date, no direct comparison between PTEN and RAD51 expression in primary prostate tumors has been reported. EXPERIMENTAL
designProstate cancer cell lines and xenografts with known PTEN status (22RV1-PTEN(+/+), DU145-PTEN(+/-), PC3-PTEN(-/-)) and H1299 and HCT116 cancer cells were used to evaluate how PTEN loss affects RAD51 expression and PARPi sensitivity. Primary prostate cancers with known PTEN status were analyzed for RAD51 expression.
resultsPTEN status is not associated with reduced RAD51 mRNA or protein expression in primary prostate cancers. Decreased PTEN expression did not reduce RAD51 expression or clonogenic survival following PARPi among prostate cancer cells that vary in TP53 and PTEN. PARPi sensitivity instead associated with a defect in MRE11 expression. PTEN-deficient cells had only mild PARPi sensitivity and no loss of HR or RAD51 recruitment. Clonogenic cell survival following a series of DNA damaging agents was variable: PTEN-deficient cells were sensitive to ionizing radiation, mitomycin-C, UV, H(2)O(2), and methyl methanesulfonate but not to cisplatin, camptothecin, or paclitaxel.
conclusionsThese data suggest that the relationship between PTEN status and survival following DNA damage is indirect and complex. It is unlikely that PTEN status will be a direct biomarker for HR status or PARPi response in prostate cancer clinical trials.
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