ArticleOncogene2004
Androgen receptor level controlled by a suppressor complex lost in an androgen-independent prostate cancer cell line.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 51 citations in OpenAlex.
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Article
- The andean anticancer herbal product BIRM causes destabilization of androgen receptor and induces caspase-8 mediated-apoptosis in prostate cancer.Oncotarget · 2016Article
- Therapeutic relevance of the protein phosphatase 2A in cancer.Oncotarget · 2016Article
- Article
- Ericifolin: a novel antitumor compound from allspice that silences androgen receptor in prostate cancer.Carcinogenesis · 2013Article
- Plk1 is upregulated in androgen-insensitive prostate cancer cells and its inhibition leads to necroptosis.Oncogene · 2013Article
- Article
- Androgen receptor gene expression in prostate cancer is directly suppressed by the androgen receptor through recruitment of lysine-specific demethylase 1.Cancer cell · 2011Article
- Regulation of HMGA1 expression by microRNA-296 affects prostate cancer growth and invasion.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- The clinical development of histone deacetylase inhibitors as targeted anticancer drugs.Expert opinion on investigational drugs · 2010Review
- HDAC6 regulates androgen receptor hypersensitivity and nuclear localization via modulating Hsp90 acetylation in castration-resistant prostate cancer.Molecular endocrinology (Baltimore, Md.) · 2009Article
- Androgen receptor expression in prostate cancer cells is suppressed by activation of epidermal growth factor receptor and ErbB2.Cancer research · 2009Article
- LEF1 in androgen-independent prostate cancer: regulation of androgen receptor expression, prostate cancer growth, and invasion.Cancer research · 2009Article
- Glucocorticoid receptor phosphorylation differentially affects target gene expression.Molecular endocrinology (Baltimore, Md.) · 2008Article
- Review
- Mithramycin targets sp1 and the androgen receptor transcription level-potential therapeutic role in advanced prostate cancer.Translational oncogenomics · 2006Article
- Histone deacetylase inhibitors: a chemical genetics approach to understanding cellular functions.Biochimica et biophysica actaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Androgen receptor (AR) overexpression is one of the characteristics of prostate cancer (PC) that progresses to hormone independence. An androgen-independent (AI) derivative, with much higher AR-mRNA and protein levels than the parental LNCaP cell line, whose proliferation was androgen dependent (AD), was used to explore the mechanism of AR overexpression. We found that a suppressor element (ARS), previously identified in mouse AR and located in the 5'-untranslated region of human AR gene, malfunctions in AI cells. Transfection of constructs that included ARS element into AD cells reduced the transactivating activities of both AR promoter and a heterologous SV40 promoter. The deletion of ARS resulted in an eightfold increase in AR-promoter activity in AD cells, but had no effect in AI cells. Moreover, the nuclear extracts of AD cells contained proteins that produced a specific, ARS-binding complex, while this complex appeared to have been lost from AI cells. Most importantly, treatment of AI cells with a demethylating agent or histone deacetylase inhibitors restored the lost ARS-binding complex. The restoration of the complex coincided with a reduced expression of AR-mRNA and protein and a reduced rate of AR-gene transcription, determined by nuclear run-on experiment. Thus, epigenetic transcriptional silencing of the suppressor protein(s) may be responsible for AR overexpression in AI cells, and its reversal in hormone-independent PC may normalize AR levels and restore their hormone dependence.
Indexed as
Identifiers
What OpenQuestion holds
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.