ArticleCancer cell2016
TRIM24 Is an Oncogenic Transcriptional Activator in Prostate Cancer.
Article in Cancer cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers, 1 of them a synthesis that pooled it.
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Who cites it
184 citing papers in PubMed, 1 synthesis or guideline pooled it, 283 citations in OpenAlex.
- The association of speckle-type POZ protein with lymph node metastasis and prognosis in cancer patients: A meta-analysis.Medicine · 2019Pooled it
- TRIM24 in Human Cancers: A Dual-Function Oncoprotein, Regulatory Mechanisms, and Emerging Therapeutic Strategies.International journal of cancer · 2026Review
- TRIM24 stabilizes the p110 CUX1 oncoprotein via USP10 to promote chemoresistance in acute myeloid leukemia.Journal of translational medicine · 2026Article
- Divergent roles of SPOP and CHD1 in ACSL4 regulation reveal context-dependent vulnerabilities for targeting ferroptosis.Nature communications · 2026Article
- Molecular determinants of AR-enhancer interaction and cistrome reprogramming in prostate cancer progression.Endocrine-related cancer · 2026Review
- Functional dissection ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- TRIM24 Regulates Adaptation to Glucose Deprivation in Association with Aspartate Accumulation and Impaired AMPK Signaling.Current issues in molecular biology · 2026Article
- Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- TRIM46 deficiency‑induced DNA damage enhances the sensitivity of cisplatin in non‑small cell lung cancer by regulating the Akt signaling pathway.Oncology reports · 2026Article
- TRIM24-mediated K27-linked ubiquitination of ULK1 alleviates energy stress-induced autophagy and promote prostate cancer growth in the context of SPOP mutation.Cell death and differentiation · 2026Article
- The Regulation of p53 by Ubiquitination and Implications for Therapeutic Targeting in Colorectal Cancer.Genes · 2026Article
- Systematic Characterization of Cancer-Associated SPOP Mutants Reveals Novel and Reprogrammable Degradative Activities.Chembiochem : a European journal of chemical biology · 2026Article
- Prognostic value of TRIM24 expression in gastric cancer and various human solid tumours: a comprehensive cross-sectional, and meta-analysis study.Przeglad gastroenterologiczny · 2026Article
- SPOP and HAUSP bidirectionally regulate LZTS2 ubiquitination to modulate the Wnt pathway.Cell death & disease · 2025Article
- High-Affinity Peptide-Drug Conjugate Ligands for the TRIM24 PHD and Bromodomain.Chemistry (Weinheim an der Bergstrasse, Germany) · 2025Article
- Simultaneous inhibition of TRIM24 and TRIM28 sensitises prostate cancer cells to antiandrogen therapy, decreasing VEGF signalling and angiogenesis.Molecular oncology · 2025Article
- Cytoplasmic TRIM24 promotes colorectal cancer cell proliferation by activating Wnt/β-catenin signaling.Nature communications · 2025Article
- TRIM24 as a therapeutic target in endocrine treatment-resistant breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- α-Cyperone affects the development and chemosensitivity of breast cancer by modulating TRIM24.In vitro cellular & developmental biology. Animal · 2025Article
124 more citing papers are in PubMed but not listed here.
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Authors and funding
22 authors at 8 institutions in 6 countries.
Funding
Abstract
Androgen receptor (AR) signaling is a key driver of prostate cancer (PC). While androgen-deprivation therapy is transiently effective in advanced disease, tumors often progress to a lethal castration-resistant state (CRPC). We show that recurrent PC-driver mutations in speckle-type POZ protein (SPOP) stabilize the TRIM24 protein, which promotes proliferation under low androgen conditions. TRIM24 augments AR signaling, and AR and TRIM24 co-activated genes are significantly upregulated in CRPC. Expression of TRIM24 protein increases from primary PC to CRPC, and both TRIM24 protein levels and the AR/TRIM24 gene signature predict disease recurrence. Analyses in CRPC cells reveal that the TRIM24 bromodomain and the AR-interacting motif are essential to support proliferation. These data provide a rationale for therapeutic TRIM24 targeting in SPOP mutant and CRPC patients.
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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.