ArticleThe Prostate2013
Androgen deprivation induces senescence characteristics in prostate cancer cells in vitro and in vivo.
Article in The Prostate, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 64 citations in OpenAlex.
- Therapeutic pressure drives the evolution of a protective ecotype characterized by AR-loss-induced senescence in prostate cancer.Theranostics · 2026Article
- Identification of a senescence-associated transcriptional program in skeletal muscle of cachectic pancreatic-tumor-bearing mice.American journal of physiology. Cell physiology · 2025Article
- 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
- Prostatic androgen receptor signaling shows an age-related and lobe-specific alteration in mice.Scientific reports · 2024Article
- Multiparametric identification of putative senescent cells in skeletal muscle via mass cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2024Article
- Modulation of tumor plasticity by senescent cells: Deciphering basic mechanisms and survival pathways to unravel therapeutic options.Genetics and molecular biology · 2024Article
- 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
- Cellular senescence in cancer: clinical detection and prognostic implications.Journal of experimental & clinical cancer research : CR · 2022Review
- Distinct mechanisms mediating therapy-induced cellular senescence in prostate cancer.Cell & bioscience · 2022Review
- Prostate cancer cells demonstrate unique metabolism and substrate adaptability acutely after androgen deprivation therapy.The Prostate · 2022Article
- Targeting senescence as an anticancer therapy.Molecular oncology · 2022Review
- Molecular environment and atypical function: What do we know about enzymes associated with Mucopolysaccharidoses?Orphanet journal of rare diseases · 2022Review
- Targeting IKKε in Androgen-Independent Prostate Cancer Causes Phenotypic Senescence and Genomic Instability.Molecular cancer therapeutics · 2022Article
- Cellular senescence as a possible link between prostate diseases of the ageing male.Nature reviews. Urology · 2021Review
- Increased CD47 and MHC Class I Inhibitory Signals Expression in Senescent CD1 Primary Mouse Lung Fibroblasts.International journal of molecular sciences · 2021Article
- Epiregulation of the SASP makes good neighbors.Nature aging · 2021Article
- Review
- Resistance to Antiandrogens in Prostate Cancer: Is It Inevitable, Intrinsic or Induced?Cancers · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe treatment of non-localized prostate cancer involves androgen deprivation (AD) therapy which results in tumor regression. Apoptosis has been implicated in the tumor response to AD, but constitutes a small fraction of the total tumor at any time. Cellular senescence is a response to sub-lethal stress in which cells are persistently growth arrested and develop distinct morphological and biochemical characteristics. The occurrence of senescence in prostate tumor tissue after AD therapy has not previously been investigated.
methodsPhenotypic and molecular characteristics of senescence were examined in models of androgen-sensitive prostate cancer after AD and compared with androgen-intact controls.
resultsIn vitro in LNCaP cells, AD induced elevated senescence-associated β-galactosidase (SA-β-gal) staining, decreased proliferation, and increased flow cytometric side scatter while minimally affecting cell viability. The increased expression of the senescence-related proteins Glb1, the cyclin-dependent kinase inhibitor p27(Kip1) and chromatin-regulating heterochromatin protein 1γ (HP1γ) were detected in LNCaP cells after AD in vitro by immunoblot and immunofluorescence microscopy. In mice bearing LuCaP xenograft tumors in vivo, surgical castration similarly increased SA-β-gal staining, increased expression of p27(Kip1) and HP1γ, and decreased expression of the proliferation marker KI-67, with minimal induction of apoptosis identified by detection of cleaved caspase 3 and TUNEL. Immunohistochemical analysis of human prostate tumors removed after AD shows similar induction of Glb1, HP1γ and decreased KI-67.
conclusionsWe conclude that AD induces characteristics consistent with cellular senescence in androgen-sensitive prostate cancer cells. This finding may explain incomplete tumor regression in response to AD.
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