ArticleMolecular endocrinology (Baltimore, Md.)2011
Hormone depletion-insensitivity of prostate cancer cells is supported by the AR without binding to classical response elements.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Aberrant expression of multiple γ-glutamyltransferases is associated with tumor progression and patient outcome in prostate cancers.Frontiers in oncology · 2025Article
- Targeting hyaluronan-mediated motility receptor (HMMR) enhances response to androgen receptor signalling inhibitors in prostate cancer.British journal of cancer · 2023Article
- African American Prostate Cancer Displays Quantitatively Distinct Vitamin D Receptor Cistrome-transcriptome Relationships Regulated by BAZ1A.Cancer research communications · 2023Article
- Identification of ELK1 interacting peptide segments in the androgen receptor.The Biochemical journal · 2022Article
- Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis.Cell reports · 2022Article
- Cell type-specific potential pathogenic genes and functional pathways in Alzheimer's Disease.BMC neurology · 2021Article
- Post-Transcriptional Regulation of PARP7 Protein Stability Is Controlled by Androgen Signaling.Cells · 2021Article
- The long non-coding RNA GHSROS reprograms prostate cancer cell lines toward a more aggressive phenotype.PeerJ · 2021Article
- CDCA2 Inhibits Apoptosis and Promotes Cell Proliferation in Prostate Cancer and Is Directly Regulated by HIF-1α Pathway.Frontiers in oncology · 2020Article
- Strategy for Tumor-Selective Disruption of Androgen Receptor Function in the Spectrum of Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Identification of Androgen Receptor Modulators in a Prostate Cancer Cell Line Microarray Compendium.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- The Amino-terminal Domain of the Androgen Receptor Co-opts Extracellular Signal-regulated Kinase (ERK) Docking Sites in ELK1 Protein to Induce Sustained Gene Activation That Supports Prostate Cancer Cell Growth.The Journal of biological chemistry · 2016Article
- The N-terminal domain of the androgen receptor drives its nuclear localization in castration-resistant prostate cancer cells.The Journal of steroid biochemistry and molecular biology · 2014Article
- The interplay of AMP-activated protein kinase and androgen receptor in prostate cancer cells.Journal of cellular physiology · 2014Article
- Deregulation of an imprinted gene network in prostate cancer.Epigenetics · 2014Article
- Article
- Patient-derived tissue slice grafts accurately depict response of high-risk primary prostate cancer to androgen deprivation therapy.Journal of translational medicine · 2013Article
- The ETS domain transcription factor ELK1 directs a critical component of growth signaling by the androgen receptor in prostate cancer cells.The Journal of biological chemistry · 2013Article
- Androgen receptor (AR) pathophysiological roles in androgen-related diseases in skin, bone/muscle, metabolic syndrome and neuron/immune systems: lessons learned from mice lacking AR in specific cells.Nuclear receptor signaling · 2013Review
- Paxillin mediates extranuclear and intranuclear signaling in prostate cancer proliferation.The Journal of clinical investigation · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
A need for androgen response elements (AREs) for androgen receptor (AR)-dependent growth of hormone depletion-insensitive prostate cancer is generally presumed. In such cells, androgen-independent activation by AR of certain genes has been attributed to selective increases in basal associations of AR with putative enhancers. We examined the importance of AR binding to DNA in prostate cancer cells in which proliferation in the absence of hormone was profoundly (∼ 90%) dependent on endogenous AR and where the receptor was not up-regulated or mutated but was predominantly nuclear. Here, ARE-mediated promoter activation and the binding of AR to a known ARE in the chromatin remained entirely androgen dependent, and the cells showed an androgen-responsive gene expression profile with an unaltered sensitivity to androgen dose. In the same cells, a different set of genes primarily enriched for cell division functions was activated by AR independently of hormone and significantly overlapped the signature gene overexpression profile of hormone ablation-insensitive clinical tumors. After knockdown of endogenous AR, hormone depletion-insensitive cell proliferation and AR apoprotein-dependent gene expression were rescued by an AR mutant that was unable to bind to ARE but that could transactivate through a well-established AR tethering protein. Hormone depletion-insensitive AR binding sites in the chromatin were functional, binding, and responding to both the wild-type and the mutant AR and lacked enrichment for canonical or noncanonical ARE half-sites. Therefore, a potentially diverse set of ARE-independent mechanisms of AR interactions with target genes must underlie truly hormone depletion-insensitive gene regulation and proliferation in prostate cancer.
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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.