ArticleProceedings of the National Academy of Sciences of the United States of America2000
Androgen-induced proliferative quiescence in prostate cancer cells: the role of AS3 as its mediator.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 92 citations in OpenAlex.
- Androgen receptor monomers and dimers regulate opposing biological processes in prostate cancer cells.Nature communications · 2024Article
- Elevated luteinizing hormone receptor signaling or selenium treatment leads to comparable changes in adrenal cortex histology and androgen-AR/ZIP9 signaling.Protoplasma · 2024Article
- Invited Perspective: Closing the Loop of Nonmonotonicity-from Natural Hormones in Experimental Endocrinology to Endocrine Disruptors in Epidemiology.Environmental health perspectives · 2024Article
- Article
- Discovery proteomics defines androgen-regulated glycoprotein networks in prostate cancer cells, as well as putative biomarkers of prostatic diseases.Scientific reports · 2021Article
- PDS5A and PDS5B in Cohesin Function and Human Disease.International journal of molecular sciences · 2021Review
- From Wingspread to CLARITY: a personal trajectory.Nature reviews. Endocrinology · 2021Review
- Studies of hormonal regulation, phenotype plasticity, bone metastasis, and experimental therapeutics in androgen-repressed human prostate cancer (ARCaP) model.American journal of clinical and experimental urology · 2021Review
- Downregulation of APRIN expression increases cancer cell proliferation via an interleukin-6/STAT3/cyclin D axis.Oncology letters · 2021Article
- The p14ARF tumor suppressor restrains androgen receptor activity and prevents apoptosis in prostate cancer cells.Cancer letters · 2020Article
- A Combined Morphometric and Statistical Approach to Assess Nonmonotonicity in the Developing Mammary Gland of Rats in the CLARITY-BPA Study.Environmental health perspectives · 2020Article
- Supraphysiological androgens suppress prostate cancer growth through androgen receptor-mediated DNA damage.The Journal of clinical investigation · 2019Article
- The Case for BPA as an Obesogen: Contributors to the Controversy.Frontiers in endocrinology · 2019Review
- The Role of Testosterone Therapy in the Setting of Prostate Cancer.Current urology reports · 2018Review
- Supraphysiological Testosterone Therapy as Treatment for Castration-Resistant Prostate Cancer.Frontiers in oncology · 2018Article
- Supraphysiologic Testosterone Therapy in the Treatment of Prostate Cancer: Models, Mechanisms and Questions.Cancers · 2017Review
- Androgen receptor differentially regulates the proliferation of prostatic epithelial cells in vitro and in vivo.Oncotarget · 2016Article
- Environmental endocrine disruptors: Effects on the human male reproductive system.Reviews in endocrine & metabolic disorders · 2015Review
- Embryonic Lethality in Homozygous Human Her-2 Transgenic Mice Due to Disruption of the Pds5b Gene.PloS one · 2015Article
- Long-range transcriptional regulation by the p110 CUX1 homeodomain protein on the ENCODE array.BMC genomics · 2013Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In the prostate gland of adult mammals, most epithelial cells are in a state of proliferative quiescence. Androgens regulate this effect by inducing cell cycle arrest in the G(0)/G(1) phase. Potential mediators of this androgen-induced proliferative shutoff were identified by means of subtracted cDNA libraries. The expression pattern of one of these sequences, AS3, strongly correlated with the expression of the androgen-induced proliferative shutoff both temporally and dosewise. The AS3 gene is located on chromosome 13 q12.3, in close proximity to the BRCA2 gene. The loss of chromosomal regions where AS3 alleles are located correlates with various human cancers, including prostate. The biological effect of AS3 was tested in two stable cell lines, one expressing sense and another expressing antisense AS3 constructs, both under tetracycline regulation. S9 cells were obtained by retroviral infection with virions containing a tetracycline-regulated sense AS3 construct. In these cells, sense AS3 was negatively regulated by tetracycline. Tetracycline withdrawal increased the expression of AS3 mRNA and protein. The expression of tetracycline-regulated AS3 resulted in inhibition of cell proliferation. A4 cells were obtained by retroviral infection with virions containing a tetracycline-regulated antisense AS3 construct. Vector-driven expression of antisense-AS3 blocked the induction of androgen-induced endogenous AS3 mRNA and blocked the inhibitory effect of androgens on cell proliferation. Tetracycline-regulated expression of the empty vector control had no effect on cell proliferation. These experiments strongly suggest that AS3 is a mediator of the androgen-induced proliferative shutoff.
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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.