ArticleNucleic acids research2023
SMAD3 promotes expression and activity of the androgen receptor in prostate cancer.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
The trial behind it
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Research progress on the role of IL‑37 in gynecological and obstetrics‑related diseases (Review).International journal of molecular medicine · 2026Review
- Polygenic risk score with KLK3 SNP-SNP interaction pairs for predicting prostate cancer aggressiveness.Communications medicine · 2026Article
- Single-nucleus sequencing dissects the malignant change of early lung adenocarcinoma: SMAD3 suppresses antitumor T cell immunity via ICAM1.NPJ precision oncology · 2026Article
- Regulation of androgen receptor expression by enhancer elements in prostate cancer.Experimental & molecular medicine · 2026Review
- Dual phosphorylation of DISC1 at Ser58 and Ser713 regulates polarization of cortical neurons via GSK3β.Science China. Life sciences · 2026Article
- Molecular mechanisms and classification of castration-resistant prostate cancer: Insights into androgen receptor, cancer stem cells, and neuroendocrine features.Current urology · 2026Article
- Radiogenomic Profiling of Prostate Tumors prior to External Beam Radiotherapy Converges on a Transcriptomic Signature of TGF-β Activity Driving Tumor Recurrence.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Observational
- BPTF regulates androgen receptor activity by enhancing chromatin accessibility and stabilizing the AR-FOXA1 interaction.Nature communications · 2025Article
- SMAD3 orchestrates RNF167 and STAMBPL1-mediated Sestrin2 ubiquitination to drive gastric cancer progression.Cell division · 2025Article
- The Sequence [RRKLPVGRS] Is a Nuclear Localization Signal for Importin 8 Binding (NLS8): A Chemical Biology and Bioinformatics Study.International journal of molecular sciences · 2025Article
- EPHB1 Protein Promoted the Progression of Prostate Adenocarcinoma Through Phosphorylating GSK3B and Activating EPHB1-GSK3B-SMAD3 Pathway.Human mutation · 2025Article
- Tackling exosome and nuclear receptor interaction: an emerging paradigm in the treatment of chronic diseases.Military Medical Research · 2024Review
- Advancing 3D Spheroid Research through 3D Scaffolds Made by Two-Photon Polymerization.Bioengineering (Basel, Switzerland) · 2024Article
- USP11 promotes prostate cancer progression by up-regulating AR and c-Myc activity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Androgen Receptor-Interacting Proteins in Prostate Cancer Development and Therapy Resistance.The American journal of pathology · 2024Review
- The mFrontiers in pharmacology · 2024Review
- Mechanism of baicalein in treatment of castration-resistant prostate cancer based on network pharmacology and cell experiments.Frontiers in pharmacology · 2024Article
- Proactive and reactive roles of TGF-β in cancer.Seminars in cancer biology · 2023Review
- SMAD Proteins in TGF-β Signalling Pathway in Cancer: Regulatory Mechanisms and Clinical Applications.Diagnostics (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Overexpression of androgen receptor (AR) is the primary cause of castration-resistant prostate cancer, although mechanisms upregulating AR transcription in this context are not well understood. Our RNA-seq studies revealed that SMAD3 knockdown decreased levels of AR and AR target genes, whereas SMAD4 or SMAD2 knockdown had little or no effect. ChIP-seq analysis showed that SMAD3 knockdown decreased global binding of AR to chromatin. Mechanistically, we show that SMAD3 binds to intron 3 of the AR gene to promote AR expression. Targeting these binding sites by CRISPRi reduced transcript levels of AR and AR targets. In addition, ∼50% of AR and SMAD3 ChIP-seq peaks overlapped, and SMAD3 may also cooperate with or co-activate AR for AR target expression. Functionally, AR re-expression in SMAD3-knockdown cells partially rescued AR target expression and cell growth defects. The SMAD3 peak in AR intron 3 overlapped with H3K27ac ChIP-seq and ATAC-seq peaks in datasets of prostate cancer. AR and SMAD3 mRNAs were upregulated in datasets of metastatic prostate cancer and CRPC compared with primary prostate cancer. A SMAD3 PROTAC inhibitor reduced levels of AR, AR-V7 and AR targets in prostate cancer cells. This study suggests that SMAD3 could be targeted to inhibit AR in prostate cancer.
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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 Socratic graph.