ArticleHormones & cancer2020
Interleukin-23 Represses the Level of Cell Senescence Induced by the Androgen Receptor Antagonists Enzalutamide and Darolutamide in Castration-Resistant Prostate Cancer Cells.
Article in Hormones & cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Induction of cellular senescence by androgen receptor agonist or antagonist is mediated via two novel common DYRK1A-DREAM and cyclin G2 signaling pathways in castration-resistant prostate cancer.Journal of advanced research · 2026Article
- Prostate Cancer: Etiology, Diagnosis, and Treatment.Serican journal of medicine · 2026Article
- The intricate interplay between circadian rhythm, androgen signaling, hormone therapy, and cellular senescence in prostate cancer.Cancer metastasis reviews · 2025Review
- The bioactivity of atraric acid as an inducer of cellular senescence in prostate cancer cells is retained by lipophilic derivatives.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The oncogenic lncRNA MIR503HG suppresses cellular senescence counteracting supraphysiological androgen treatment in prostate cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Functional circuits of LYL1 controlled by supraphysiological androgen in prostate cancer cells to regulate cell senescence.Cell communication and signaling : CCS · 2024Article
- The clock gene BHLHE40 and atypical CCNG2 control androgen-induced cellular senescence as a novel tumor suppressive pathway in prostate cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- The protein composition of exosomes released by prostate cancer cells is distinctly regulated by androgen receptor-antagonists and -agonist to stimulate growth of target cells.Cell communication and signaling : CCS · 2024Article
- A new perspective on prostate cancer treatment: the interplay between cellular senescence and treatment resistance.Frontiers in immunology · 2024Review
- Baicalin Antagonizes Prostate Cancer Stemness via Inhibiting Notch1/NF-κB Signaling Pathway.Chinese journal of integrative medicine · 2023Article
- Let's Go 3D! New Generation of Models for Evaluating Drug Response and Resistance in Prostate Cancer.International journal of molecular sciences · 2023Review
- Distinct mechanisms mediating therapy-induced cellular senescence in prostate cancer.Cell & bioscience · 2022Review
- The tumor innate immune microenvironment in prostate cancer: an overview of soluble factors and cellular effectors.Exploration of targeted anti-tumor therapy · 2022Review
- Serine and one-carbon metabolisms bring new therapeutic venues in prostate cancer.Discover oncology · 2021Review
- Anti-Proliferative, Anti-Angiogenic and Safety Profiles of Novel HDAC Inhibitors for the Treatment of Metastatic Castration-Resistant Prostate Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Article
- Response to Androgens and Androgen Receptor Antagonists in the Presence of Cytokines in Prostate Cancer.Cancers · 2021Review
- Recent Research Progress of Chiral Small Molecular Antitumor-Targeted Drugs Approved by the FDA From 2011 to 2019.Frontiers in oncology · 2021Review
- Mechanisms of Androgen Receptor Agonist- and Antagonist-Mediated Cellular Senescence in Prostate Cancer.Cancers · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PCa) is the most common cancer and the second leading cause of cancer-related deaths of men in Western countries. Androgen deprivation therapy is initially successful, however eventually fails, and tumors progress to the more aggressive castration-resistant PCa (CRPC). Yet, androgen receptor (AR) usually remains as a major regulator of tumor cell proliferation in CRPC. Interleukin-23 (IL-23) was recently shown to promote the development of CRPC by driving AR transcription. Here we used the androgen-sensitive LNCaP, castration-resistant C4-2, and 22Rv1 cells. Interestingly, cellular senescence is induced in these human cell lines by treatment with the AR antagonists enzalutamide (ENZ) or darolutamide (ODM), which might be one underlying mechanism for inhibition of PCa cell proliferation. Treatment with IL-23 alone did not change cellular senescence levels in these cell lines, whereas IL-23 inhibited significantly cellular senescence levels induced by ENZ or ODM in both CRPC cell lines C4-2 and 22Rv1 but not in LNCaP cells. This indicates a response of IL-23 specific in CRPC cells. Generating LNCaP and C4-2 three-dimensional (3D) spheroids and treatment with AR antagonists resulted in the reduced spheroid volume and thus growth inhibition. However, the combination of AR antagonists with IL-23 did not affect the antagonist-mediated reduction of spheroid volumes. This observation was confirmed with proliferation assays using adherent monolayer cell cultures. Taken together, the data indicate that IL-23 treatment reduces the AR antagonists-induced level of cellular senescence of CRPC cells, which could be one possible mechanism for promoting castration resistance.
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