ArticleCancer research2017
Polycomb-Mediated Disruption of an Androgen Receptor Feedback Loop Drives Castration-Resistant Prostate Cancer.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Amino-truncated NOV expression and its correlation with clinicopathologic features, prognosis, metastasis, and chemoresistance in bladder cancer.Cancer biology & therapy · 2024Article
- Pleckstrin-2 Mediates the Activation of AKT in Prostate Cancer and Is Repressed by Androgen Receptor.The American journal of pathology · 2024Article
- Dual-target EZH2 inhibitor: latest advances in medicinal chemistry.Future medicinal chemistry · 2024Review
- Calcium signalling pathways in prostate cancer initiation and progression.Nature reviews. Urology · 2023Review
- High intratumoral dihydrotestosterone is associated with antiandrogen resistance in VCaP prostate cancer xenografts in castrated mice.iScience · 2022Article
- The CCN axis in cancer development and progression.Journal of cell communication and signaling · 2021Review
- Cellular communication network factor 3 in cartilage development and maintenance.Journal of cell communication and signaling · 2021Review
- Identification of Androgen Receptor Metabolic Correlome Reveals the Repression of Ceramide Kinase by Androgens.Cancers · 2021Article
- PVT1 signals an androgen-dependent transcriptional repression program in prostate cancer cells and a set of the repressed genes predicts high-risk tumors.Cell communication and signaling : CCS · 2021Article
- Posttranslational regulation of androgen dependent and independent androgen receptor activities in prostate cancer.Asian journal of urology · 2020Review
- Cellular and Molecular Mechanisms Underlying Prostate Cancer Development: Therapeutic Implications.Medicines (Basel, Switzerland) · 2019Review
- Molecules targeting the androgen receptor (AR) signaling axis beyond the AR-Ligand binding domain.Medicinal research reviews · 2019Review
- Interaction Of c-Jun And HOTAIR- Increased Expression Of p21 Converge In Polyphyllin I-Inhibited Growth Of Human Lung Cancer Cells.OncoTargets and therapy · 2019Article
- Genomics of sex hormone receptor signaling in hepatic sexual dimorphism.Molecular and cellular endocrinology · 2018Article
- CCN3-EZH2-AR feedback loop: new targets for enzalutamide and castration resistant prostate cancer.Journal of cell communication and signaling · 2017Article
- Transcriptional repression by androgen receptor: roles in castration-resistant prostate cancer.Asian journal of andrologyReview
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The lethal phenotype of castration-resistant prostate cancer (CRPC) is generally caused by augmented signaling from the androgen receptor (AR). Here, we report that the AR-repressed gene CCN3/NOV inhibits AR signaling and acts in a negative feedback loop to block AR function. Mechanistically, a cytoplasmic form of CCN3 interacted with the AR N-terminal domain to sequester AR in the cytoplasm of prostate cancer cells, thereby reducing AR transcriptional activity and inhibiting cell growth. However, constitutive repression of CCN3 by the Polycomb group protein EZH2 disrupted this negative feedback loop in both CRPC and enzalutamide-resistant prostate cancer cells. Notably, restoring CCN3 was sufficient to effectively reduce CPRC cell proliferation in vitro and to abolish xenograft tumor growth in vivo Taken together, our findings establish CCN3 as a pivotal regulator of AR signaling and prostate cancer progression and suggest a functional intersection between Polycomb and AR signaling in CRPC. Cancer Res; 77(2); 412-22. ©2016 AACR.
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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.