ArticleNature communications2018
Heterozygous deletion of chromosome 17p renders prostate cancer vulnerable to inhibition of RNA polymerase II.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- Rezvilutamide plus docetaxel in chemotherapy-naive metastatic castration-resistant prostate cancer patients after progression on abiraterone: A multi-centre, open-label, phase II trial.Clinical and translational medicine · 2026Trial
- CRISPR decodes the RNA regulatory network in prostate cancer: A review from mechanisms to precision therapeutics.Non-coding RNA research · 2026Review
- Article
- USP10 Inhibits Ferroptosis via Deubiquinating POLR2A in Head and Neck Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The class II myosin MYH4 safeguards genome integrity and suppresses tumor progression.The Journal of clinical investigation · 2025Article
- Deletion of 17p in cancers: Guilt by (p53) association.Oncogene · 2025Review
- The Role of p53 Mutations in Early and Late Response to Mitotic Aberrations.Biomolecules · 2025Review
- Advances in Immunotherapy for HER2 Low-Expressing Triple-Negative Breast Cancer.Cancer management and research · 2025Review
- Transcriptional rewiring in cancer driven byFrontiers in pharmacology · 2025Review
- Aneuploidy as a driver of human cancer.Nature genetics · 2024Review
- Transforming toxins into treatments: the revolutionary role of α-amanitin in cancer therapy.Archives of toxicology · 2024Review
- Identification and validation of a novel anoikis-related prognostic model for prostate cancer.Molecular genetics & genomic medicine · 2024Article
- Article
- ARMC5 controls the degradation of most Pol II subunits, and ARMC5 mutation increases neural tube defect risks in mice and humans.Genome biology · 2024Article
- Novel Anti-B-cell Maturation Antigen Alpha-Amanitin Antibody-drug Conjugate HDP-101 Shows Superior Activity to Belantamab Mafodotin and Enhanced Efficacy in Deletion 17p Myeloma Models.Research square · 2024Article
- Prostate tumor markers: diagnosis, prognosis and management.Genetics and molecular biology · 2024Article
- Stressed target cancer cells drive nongenetic reprogramming of CAR T cells and solid tumor microenvironment.Nature communications · 2023Article
- A T Cell-Engaging Tumor Organoid Platform for Pancreatic Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Castration-resistant prostate cancer cells are dependent on the high activity of CDK7.Journal of cancer research and clinical oncology · 2023Article
- Role of K63-linked ubiquitination in cancer.Cell death discovery · 2022Review
Corrections and comments
- Retracted
Authors and funding
22 authors at 9 institutions in 2 countries.
Funding
Abstract
Heterozygous deletion of chromosome 17p (17p) is one of the most frequent genomic events in human cancers. Beyond the tumor suppressor TP53, the POLR2A gene encoding the catalytic subunit of RNA polymerase II (RNAP2) is also included in a ~20-megabase deletion region of 17p in 63% of metastatic castration-resistant prostate cancer (CRPC). Using a focused CRISPR-Cas9 screen, we discovered that heterozygous loss of 17p confers a selective dependence of CRPC cells on the ubiquitin E3 ligase Ring-Box 1 (RBX1). RBX1 activates POLR2A by the K63-linked ubiquitination and thus elevates the RNAP2-mediated mRNA synthesis. Combined inhibition of RNAP2 and RBX1 profoundly suppress the growth of CRPC in a synergistic manner, which potentiates the therapeutic effectivity of the RNAP2 inhibitor, α-amanitin-based antibody drug conjugate (ADC). Given the limited therapeutic options for CRPC, our findings identify RBX1 as a potentially therapeutic target for treating human CRPC harboring heterozygous deletion of 17p.
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Identifiers
What OpenQuestion holds
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.