ArticleNeoplasia (New York, N.Y.)2008
Inhibition of glycogen synthase kinase-3 in androgen-responsive prostate cancer cell lines: are GSK inhibitors therapeutically useful?
Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
28 citing papers in PubMed, 45 citations in OpenAlex.
- The Androgen Hormone-Induced Increase in Androgen Receptor Protein Expression Is Caused by the Autoinduction of the Androgen Receptor Translational Activity.Current issues in molecular biology · 2022Article
- Glycogen synthase kinase 3β in tumorigenesis and oncotherapy (Review).Oncology reports · 2020Review
- Review
- Review
- A nuclear shift of GSK3β protein is an independent prognostic factor in prostate cancer.Oncotarget · 2019Article
- Impaired Nuclear Export of Polyglutamine-Expanded Androgen Receptor in Spinal and Bulbar Muscular Atrophy.Scientific reports · 2019Article
- A novel role for GSK3β as a modulator of Drosha microprocessor activity and MicroRNA biogenesis.Nucleic acids research · 2017Article
- 6BIO Enhances Oligonucleotide Activity in Cells: A Potential Combinatorial Anti-androgen Receptor Therapy in Prostate Cancer Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- GSK-3β controls NF-kappaB activity via IKKγ/NEMO.Scientific reports · 2016Article
- Modulation of glycogen synthase kinase-3β following TRAIL combinatorial treatment in cancer cells.Oncotarget · 2016Article
- Wnt signalling is a bi-directional vulnerability of cancer cells.Oncotarget · 2016Article
- Glycogen synthase kinase-3: a potential preventive target for prostate cancer management.Urologic oncology · 2015Review
- Does Wnt/β-catenin pathway contribute to the stability of DNMT1 expression in urological cancer cell lines?Experimental biology and medicine (Maywood, N.J.) · 2015Article
- Discrete functions of GSK3α and GSK3β isoforms in prostate tumor growth and micrometastasis.Oncotarget · 2015Article
- Androgen receptor (AR) inhibitor ErbB3-binding protein-1 (Ebp1) is not targeted by the newly identified AR controlling signaling axis heat-shock protein HSP27 and microRNA miR-1 in prostate cancer cells.World journal of urology · 2015Article
- Article
- The fibroblast growth factor 14·voltage-gated sodium channel complex is a new target of glycogen synthase kinase 3 (GSK3).The Journal of biological chemistry · 2013Article
- Glycogen synthase kinase-3β is involved in ligand-dependent activation of transcription and cellular localization of the glucocorticoid receptor.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Combined Treatment of Androgen-Independent Prostate Cancer Cell Line DU145 with Chemotherapeutic Agents and Lithium Chloride: Effect on Growth Arrest and/or Apoptosis.Avicenna journal of medical biotechnology · 2012Article
- Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glycogen synthase kinase 3 (GSK-3) is a serine/threonine kinase widely expressed in mammalian tissues. Initially identified by its ability to modulate glycogen synthesis, GSK-3 turned out to be a multifunctional enzyme, able to phosphorylate many proteins, including members of the steroid receptor superfamily. Although GSK-3 was shown to phosphorylate the androgen receptor (AR), its effects on AR transcriptional activity remain controversial. Analysis of short hairpin RNA (shRNA)-mediated downmodulation of GSK-3 proteins in prostate cancer cells showed a reduction in AR transcriptional activity and AR protein levels. Pharmacological GSK-3 inhibitors such as the maleimide SB216763 or the aminopyrazole GSK inhibitor XIII inhibited AR-dependent reporter gene activity and AR expression in vitro. Analysis of androgen-induced nuclear translocation of the AR was performed in PC3 cells transfected with pAR-t1EosFP coding for EosAR, a green fluorescent AR fusion protein. When grown in presence of androgens, EosAR was predominantly nuclear. Incubation with SB216763 before and after androgen treatment almost completely reduced nuclear EosAR. In contrast, the thiazole-containing urea compound AR-A014418 increased rather than decreased AR-expression/function. Although not all GSK inhibitors affected AR-stability/function, our observations suggest a potential new therapeutic application for some of these compounds in prostate cancer.
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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.