ArticleEndocrinology2012
Nuclear export signal of androgen receptor (NESAR) regulation of androgen receptor level in human prostate cell lines via ubiquitination and proteasome-dependent degradation.
Article in Endocrinology, 2012. 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, 31 citations in OpenAlex.
- Differentially disrupted spinal cord and muscle energy metabolism in spinal and bulbar muscular atrophy.JCI insight · 2024Article
- Review
- Androgen receptor nucleocytoplasmic trafficking - A one-way journey.Molecular and cellular endocrinology · 2023Review
- Mechanisms and targeting of proteosome-dependent androgen receptor degradation in prostate cancer.American journal of clinical and experimental urology · 2022Review
- The role of ubiquitination in spinal and bulbar muscular atrophy.Frontiers in molecular neuroscience · 2022Review
- Regulation and targeting of androgen receptor nuclear localization in castration-resistant prostate cancer.The Journal of clinical investigation · 2021Article
- The classical and updated models of androgen receptor nucleocytoplasmic trafficking.American journal of clinical and experimental urology · 2021Review
- SUMO3 modification by PIAS1 modulates androgen receptor cellular distribution and stability.Cell communication and signaling : CCS · 2019Article
- Molecular Mechanisms and Therapeutics for SBMA/Kennedy's Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- The tumor suppressor OVCA1 is a short half-life protein degraded by the ubiquitin-proteasome pathway.Oncology letters · 2019Article
- Impaired Nuclear Export of Polyglutamine-Expanded Androgen Receptor in Spinal and Bulbar Muscular Atrophy.Scientific reports · 2019Article
- DHX15 promotes prostate cancer progression by stimulating Siah2-mediated ubiquitination of androgen receptor.Oncogene · 2018Article
- Inhibition of Androgen Receptor Nuclear Localization and Castration-Resistant Prostate Tumor Growth by Pyrroloimidazole-based Small Molecules.Molecular cancer therapeutics · 2017Article
- Inhibition of Androgen Receptor Function and Level in Castration-Resistant Prostate Cancer Cells by 2-[(isoxazol-4-ylmethyl)thio]-1-(4-phenylpiperazin-1-yl)ethanone.Endocrinology · 2017Article
- Allosteric alterations in the androgen receptor and activity in prostate cancer.Endocrine-related cancer · 2017Review
- Reciprocal stabilization of ABL and TAZ regulates osteoblastogenesis through transcription factor RUNX2.The Journal of clinical investigation · 2016Article
- Splicing Factor Prp8 Interacts With NES(AR) and Regulates Androgen Receptor in Prostate Cancer Cells.Molecular endocrinology (Baltimore, Md.) · 2015Article
- The link between androgen receptor splice variants and castration-resistant prostate cancer.Hormones & cancer · 2014Review
- Preclinical evaluation of the supercritical extract of azadirachta indica (neem) leaves in vitro and in vivo on inhibition of prostate cancer tumor growth.Molecular cancer therapeutics · 2014Article
- Posttranslational modification of the androgen receptor in prostate cancer.International journal of molecular sciences · 2013Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Androgen receptor (AR) plays a key role in prostate development and carcinogenesis. Increased expression and/or stability of AR is associated with sensitization of prostate cancer cells to low levels of androgens, leading to castration resistance. Hence, understanding the mechanisms regulating AR protein stability is clinically relevant and may lead to new approaches to prevent and/or treat prostate cancer. Using fluorescence microscopy, Western blot, and pulse chase assay, we showed that nuclear export signal (NES)(AR), a nuclear export signal in the ligand binding domain (LBD) of AR, can significantly enhance the degradation of fusion protein constructs in PC3 prostate cancer cells. The half-life of GFP-NES(AR) was less than 3 h, which was 10 times shorter than that of green fluorescent protein (GFP) control. Further analysis showed that NES(AR) can signal for polyubiquitination and that degradation of NES(AR)-containing fusion proteins can be blocked by proteasome inhibitor MG132. Ubiquitination of GFP-AR or GFP-LBD was suppressed in the presence of dihydrotestosterone, which is known to suppress NES(AR) while inducing nuclear localization signal 2 in AR or LBD, suggesting that the export activity of NES(AR) is required for NES(AR)-mediated polyubiquitination. Treatment with MG132 also induced aggresome formation of NES(AR)-containing fusion proteins in perinuclear regions of the transfected PC3 cells, indicating a role for NES(AR) in inducing unfolded protein responses. The above observations suggest that NES(AR) plays a key role in AR ubiquitination and proteasome-dependent degradation 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.