ReviewCells2020
Targeting the RNA Polymerase I Transcription for Cancer Therapy Comes of Age.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 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
108 citing papers in PubMed, 184 citations in OpenAlex.
- Transcription termination factor 2 (TTF2) prevents premature rRNA synthesis during mitotic exit.Life science alliance · 2026Article
- Novel RNA polymerase I and cyclin-dependent kinase combination therapy for the treatment of aggressive acute myeloid leukemia.Leukemia · 2026Article
- JP-1302 inhibits RNA polymerase I transcription and induces nucleolar stress in cancer cell lines.Cell death discovery · 2026Article
- In vivo CRISPR knockout screen identifies Polr1a as a key driver and a potential therapeutic target for melanoma metastasis.Oncogene · 2026Article
- [Advances in ribosome biogenesis and targeted therapies for diffuse large B-cell lymphomas].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Review
- Copper Complexes: Main Mechanisms as Anticancer Agents.Molecules (Basel, Switzerland) · 2026Review
- Dynamic landscape of transcription initiation by yeast RNA polymerase I.Nucleic acids research · 2026Article
- Loss of p53 Provokes NF-κB-Dependent Disruption of Nucleolar Cap and Nucleoplasmic Redistribution of Fibrillarin During Nucleolar Stress.Biomolecules · 2026Article
- Signaling to make human ribosomes: Connections between the cytoplasm and the nucleolus.Molecular cell · 2026Review
- In silico mapping of non-canonical DNA structures across the human ribosomal DNA locus.G3 (Bethesda, Md.) · 2026Article
- Ubiquitination of Oncogenic Mutant p53 via Attenuation of Ribosome Biogenesis Machinery Effectively Inhibits Pancreatic Tumor Growth.Molecular cancer therapeutics · 2026Article
- Early growth response 1 promotes RNA polymerase I-directed transcription and cancer growth by activating RRN3 expression.Communications biology · 2026Article
- SPRTN preserves RNA polymerase I transcription under genotoxic drug stress in lung adenocarcinoma.Frontiers in oncology · 2026Article
- Synthetic messenger RNA vaccines and transcriptomic dysregulation: Evidence from new-onset adverse events and cancers post-vaccination.World journal of experimental medicine · 2025Article
- Dual RNA Polymerase I Inhibition with CX-5461 and BMH-21 Synergizes in Breast Cancer by Activating p53-Dependent Stress.bioRxiv : the preprint server for biology · 2025Article
- Fibrillarin-mediated ribosomal RNA maturation is a novel therapeutic vulnerability in triple-negative breast cancer.Breast cancer research : BCR · 2025Article
- NSH76: a selective inhibitor of RRN3 and RNA polymerase I transcription with potential for cancer therapy.Journal of translational medicine · 2025Article
- Lysosomal membrane permeabilization enhances the anticancer effects of POLR1 (RNA polymerase I) transcription inhibitors.Autophagy · 2025Article
- Review
- Nonchromatin regulatory functions of the histone variant H2A.B in SWI/SNF genomic deposition.Science advances · 2025Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
Transcription of the ribosomal RNA genes (rDNA) that encode the three largest ribosomal RNAs (rRNA), is mediated by RNA Polymerase I (Pol I) and is a key regulatory step for ribosomal biogenesis. Although it has been reported over a century ago that the number and size of nucleoli, the site of ribosome biogenesis, are increased in cancer cells, the significance of this observation for cancer etiology was not understood. The realization that the increase in rRNA expression has an active role in cancer progression, not only through increased protein synthesis and thus proliferative capacity but also through control of cellular check points and chromatin structure, has opened up new therapeutic avenues for the treatment of cancer through direct targeting of Pol I transcription. In this review, we discuss the rational of targeting Pol I transcription for the treatment of cancer; review the current cancer therapeutics that target Pol I transcription and discuss the development of novel Pol I-specific inhibitors, their therapeutic potential, challenges and future prospects.
Indexed as
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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.