ArticlePloS one2013
Androgen deprivation-induced senescence promotes outgrowth of androgen-refractory prostate cancer cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The trial behind it
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
39 citing papers in PubMed, 63 citations in OpenAlex.
- Ki67 Is an Independent Predictor of Recurrence in the Largest Randomized Trial of 3 Radiation Fractionation Schedules in Localized Prostate Cancer.International journal of radiation oncology, biology, physics · 2018Trial
- Senolytic Interventions Enhance the Anti-metastatic Activity of Chemotherapy in Prostate Cancer.Cancer research · 2026Article
- ARv7 promotes the escape of prostate cancer cells from androgen deprivation therapy-induced senescence by mediating the SKP2/p27 axis.BMC biology · 2025Article
- Stimulating Soluble Guanylyl Cyclase with the Clinical Agonist Riociguat Restrains the Development and Progression of Castration-Resistant Prostate Cancer.Cancer research · 2025Article
- A new perspective on prostate cancer treatment: the interplay between cellular senescence and treatment resistance.Frontiers in immunology · 2024Review
- A GATA2-CDC6 axis modulates androgen receptor blockade-induced senescence in prostate cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- Androgen Deprivation Freezes Hormone-Sensitive Prostate Cancer Cells in a Reversible, Genetically Unstable Quasi-Apoptotic State, Bursting into Full Apoptosis upon Poly(ADP-ribose) Polymerase Inhibition.International journal of molecular sciences · 2023Article
- Distinct mechanisms mediating therapy-induced cellular senescence in prostate cancer.Cell & bioscience · 2022Review
- Targeting senescence as an anticancer therapy.Molecular oncology · 2022Review
- SARS-CoV-2 spike S1 subunit protein-mediated increase of beta-secretase 1 (BACE1) impairs human brain vessel cells.Biochemical and biophysical research communications · 2022Article
- Article
- SIRT1 inhibition-induced senescence as a strategy to prevent prostate cancer progression.Molecular carcinogenesis · 2022Article
- Hypoxic Signaling Is Modulated by Calcium Channel, CaV1.3, in Androgen-Resistant Prostate Cancer.Bioelectricity · 2022Article
- PPFIA4 promotes castration-resistant prostate cancer by enhancing mitochondrial metabolism through MTHFD2.Journal of experimental & clinical cancer research : CR · 2022Article
- Targeting IKKε in Androgen-Independent Prostate Cancer Causes Phenotypic Senescence and Genomic Instability.Molecular cancer therapeutics · 2022Article
- Targeting the Intrinsic Apoptosis Pathway: A Window of Opportunity for Prostate Cancer.Cancers · 2021Review
- Article
- Cellular Senescence: Mechanisms and Therapeutic Potential.Biomedicines · 2021Review
- A draft genome, resequencing, and metabolomes reveal the genetic background and molecular basis of the nutritional and medicinal properties of loquat (Eriobotrya japonica (Thunb.) Lindl).Horticulture research · 2021Article
- Adaptive response of resistant cancer cells to chemotherapy.Cancer biology & medicine · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgen deprivation (AD) is an effective method for initially suppressing prostate cancer (PC) progression. However, androgen-refractory PC cells inevitably emerge from the androgen-responsive tumor, leading to incurable disease. Recent studies have shown AD induces cellular senescence, a phenomenon that is cell-autonomously tumor-suppressive but which confers tumor-promoting adaptations that can facilitate the advent of senescence-resistant malignant cell populations. Because androgen-refractory PC cells emerge clonally from the originally androgen-responsive tumor, we sought to investigate whether AD-induced senescence (ADIS) affects acquisition of androgen-refractory behavior in androgen-responsive LNCaP and LAPC4 prostate cancer cells. We find that repeated exposure of these androgen-responsive cells to senescence-inducing stimuli via cyclic AD leads to the rapid emergence of ADIS-resistant, androgen-refractory cells from the bulk senescent cell population. Our results show that the ADIS phenotype is associated with tumor-promoting traits, notably chemoresistance and enhanced pro-survival mechanisms such as inhibition of p53-mediated cell death, which encourage persistence of the senescent cells. We further find that pharmacologic enforcement of p53/Bax activation via Nutlin-3 prior to establishment of ADIS is required to overcome the associated pro-survival response and preferentially trigger pervasive cell death instead of senescence during AD. Thus our study demonstrates that ADIS promotes outgrowth of androgen-refractory PC cells and is consequently a suboptimal tumor-suppressor response to AD.
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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.