ArticlePloS one2011
FUS/TLS is a co-activator of androgen receptor in prostate cancer cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Disruption of androgen receptor-cofactor interactions by the RNA-binding protein FUS/TLS alters androgen signalling in prostate cancer.Oncogene · 2026Article
- Complementary analysis of proteome-wide proteomics reveals changes in RNA binding protein-profiles during prostate cancer progression.Cancer reports (Hoboken, N.J.) · 2023Article
- DNA-binding domain as the minimal region driving RNA-dependent liquid-liquid phase separation of androgen receptor.Protein science : a publication of the Protein Society · 2021Article
- Interaction of BACH2 with FUS promotes malignant progression of glioma cells via the TSLNC8-miR-10b-5p-WWC3 pathway.Molecular oncology · 2020Article
- Lysine acetylation regulates the RNA binding, subcellular localization and inclusion formation of FUS.Human molecular genetics · 2020Article
- MiR-133a-5p inhibits androgen receptor (AR)-induced proliferation in prostate cancer cells via targeting FUsed in Sarcoma (FUS) and AR.Cancer biology & therapy · 2020Article
- Novel Function of lncRNA ADAMTS9-AS2 in Promoting Temozolomide Resistance in Glioblastoma via Upregulating the FUS/MDM2 Ubiquitination Axis.Frontiers in cell and developmental biology · 2019Article
- Elevated FUS/TLS expression is negatively associated with E-cadherin expression and prognosis of patients with non-small cell lung cancer.Oncology letters · 2018Article
- FUS interacts with nuclear matrix-associated protein SAFB1 as well as Matrin3 to regulate splicing and ligand-mediated transcription.Scientific reports · 2016Article
- Proteomic analysis of FUS interacting proteins provides insights into FUS function and its role in ALS.Biochimica et biophysica acta · 2016Article
- IDH1 mutation-associated long non-coding RNA expression profile changes in glioma.Journal of neuro-oncology · 2015Article
- Identification, by systematic RNA sequencing, of novel candidate biomarkers and therapeutic targets in human soft tissue tumors.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- The impact of point mutations in the human androgen receptor: classification of mutations on the basis of transcriptional activity.PloS one · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Androgen receptor (AR) is a member of the nuclear receptor family of transcription factors. Upon binding to androgens, AR becomes transcriptionally active to regulate the expression of target genes that harbor androgen response elements (AREs) in their promoters and/or enhancers. AR is essential for the growth and survival of prostate cancer cells and is therefore a target for current and next-generation therapeutic modalities against prostate cancer. Pathophysiologically relevant protein-protein interaction networks involving AR are, however, poorly understood. In this study, we identified the protein FUsed/Translocated in LipoSarcoma (FUS/TLS) as an AR-interacting protein by co-immunoprecipitation of endogenous proteins in LNCaP human prostate cancer cells. The hormonal response of FUS expression in LNCaP cells was shown to resemble that of other AR co-activators. FUS displayed a strong intrinsic transactivation capacity in prostate cancer cells when tethered to basal promoters using the GAL4 system. Chromatin immunoprecipitation experiments showed that FUS was recruited to ARE III of the enhancer region of the PSA gene. Data from ectopic overexpression and "knock-down" approaches demonstrated that AR transcriptional activity was enhanced by FUS. Depletion of FUS reduced androgen-dependent proliferation of LNCaP cells. Thus, FUS is a novel co-activator of AR in prostate cancer cells.
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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.