ArticleBiochemical and biophysical research communications2013
Androgen receptor primes prostate cancer cells to apoptosis through down-regulation of basal p21 expression.
Article in Biochemical and biophysical research communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Bipolar Androgen Therapy: When Excess Fuel Extinguishes the Fire.Biomedicines · 2023Review
- Alternations of gene expression in PI3K and AR pathways and DNA methylation features contribute to metastasis of prostate cancer.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- Delineation of the androgen-regulated signaling pathways in prostate cancer facilitates the development of novel therapeutic approaches.Current opinion in pharmacology · 2018Review
- Supraphysiologic Testosterone Therapy in the Treatment of Prostate Cancer: Models, Mechanisms and Questions.Cancers · 2017Review
- Article
- Androgen receptor (AR) positive vs negative roles in prostate cancer cell deaths including apoptosis, anoikis, entosis, necrosis and autophagic cell death.Cancer treatment reviews · 2014Review
- Androgen receptor coactivators that inhibit prostate cancer growth.American journal of clinical and experimental urology · 2014Review
- Decreased tumorigenesis and mortality from bladder cancer in mice lacking urothelial androgen receptor.The American journal of pathology · 2013Article
- Androgen receptor in human prostate cancer-associated fibroblasts promotes prostate cancer epithelial cell growth and invasion.Medical oncology (Northwood, London, England) · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The androgen receptor (AR) for the male hormone androgen plays an important role in regulation of cell survival or death depending on the nature of cellular context and extracellular stimuli. The pro-survival function of AR is mediated mainly by transcriptional regulation of its target genes. By contrast, the pro-death function of AR can be transcription-dependent or -independent, although the underlying mechanism of the latter is incompletely understood. Here we report that, in androgen-independent prostate cancer cells, AR promotes UV-induced apoptosis through down-regulation of basal expression of p21 independently of its transcriptional activity. Down-regulation of basal p21 expression depends on AR N-terminal interacting protein PIRH2, an E3 ligase for proteasomal degradation of p53. Silencing of PIRH2 up-regulates p53, which in turn activates p21 transcription. Consistent with this, knockdown of PIRH2 suppresses UV-induced AR-dependent apoptosis. Our data suggest that AR primes androgen-independent prostate cancer cells to DNA damage-induced apoptosis through the PIRH2-p53-p21 axis.
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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.