ArticlePloS one2010
beta-TrCP inhibition reduces prostate cancer cell growth via upregulation of the aryl hydrocarbon receptor.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Structural Studies of βTrCP Reveal Plasticity in Binding Modes of Consensus and Nonconsensus Degrons.ACS chemical biology · 2026Article
- The Kynurenine Pathway and Indole Pathway in Tryptophan Metabolism Influence Tumor Progression.Cancer medicine · 2025Review
- Review
- Potential Role of Host Microbiome in Areca Nut-Associated Carcinogenesis and Addiction.Molecules (Basel, Switzerland) · 2022Review
- WBP2 promotes BTRC mRNA stability to drive migration and invasion in triple-negative breast cancer via NF-κB activation.Molecular oncology · 2022Article
- Post-Translational Modifications That Drive Prostate Cancer Progression.Biomolecules · 2021Review
- Epigenetic Regulations of AhR in the Aspect of Immunomodulation.International journal of molecular sciences · 2020Review
- Kynurenic acid and cancer: facts and controversies.Cellular and molecular life sciences : CMLS · 2020Review
- Correlation of the Aryl Hydrocarbon Receptor with FSHR in Ovarian Cancer Patients.International journal of molecular sciences · 2019Article
- Overexpression of aryl hydrocarbon receptor (AHR) signalling pathway in human meningioma.Journal of neuro-oncology · 2018Article
- Article
- β-transducin repeat-containing E3 ubiquitin protein ligase inhibits migration, invasion and proliferation of glioma cells.Oncology letters · 2017Article
- The Complex Biology of the Aryl Hydrocarbon Receptor and Its Role in the Pituitary Gland.Hormones & cancer · 2017Review
- Role of the aryl hydrocarbon receptor in carcinogenesis and potential as an anti-cancer drug target.Archives of toxicology · 2017Review
- The inhibition of lung cancer cell migration by AhR-regulated autophagy.Scientific reports · 2017Article
- The Aryl Hydrocarbon Receptor (AhR) as a Drug Target for Cancer Chemotherapy.Current opinion in toxicology · 2017Article
- REST reduction is essential for hypoxia-induced neuroendocrine differentiation of prostate cancer cells by activating autophagy signaling.Oncotarget · 2016Article
- Hint1 Up-Regulates IκBα by Targeting the β-TrCP Subunit of SCF E3 Ligase in Human Hepatocellular Carcinoma Cells.Digestive diseases and sciences · 2016Article
- EBV-miR-BART10-3p facilitates epithelial-mesenchymal transition and promotes metastasis of nasopharyngeal carcinoma by targeting BTRC.Oncotarget · 2015Article
- A rapid screening system evaluates novel inhibitors of DNA methylation and suggests F-box proteins as potential therapeutic targets for high-risk neuroblastoma.Targeted oncology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProstate cancer is a common and heterogeneous disease, where androgen receptor (AR) signaling plays a pivotal role in development and progression. The initial treatment for advanced prostate cancer is suppression of androgen signaling. Later on, essentially all patients develop an androgen independent stage which does not respond to anti hormonal treatment. Thus, alternative strategies targeting novel molecular mechanisms are required. beta-TrCP is an E3 ligase that targets various substrates essential for many aspects of tumorigenesis. METHODOLOGY/PRINCIPAL
findingsHere we show that beta-TrCP depletion suppresses prostate cancer and identify a relevant growth control mechanism. shRNA targeted against beta-TrCP reduced prostate cancer cell growth and cooperated with androgen ablation in vitro and in vivo. We found that beta-TrCP inhibition leads to upregulation of the aryl hydrocarbon receptor (AhR) mediating the therapeutic effect. This phenomenon could be ligand independent, as the AhR ligand 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) did not alter prostate cancer cell growth. We detected high AhR expression and activation in basal cells and atrophic epithelial cells of human cancer bearing prostates. AhR expression and activation is also significantly higher in tumor cells compared to benign glandular epithelium. CONCLUSIONS/SIGNIFICANCE: Together these observations suggest that AhR activation may be a cancer counteracting mechanism in the prostate. We maintain that combining beta-TrCP inhibition with androgen ablation could benefit advanced prostate cancer patients.
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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.