ReviewOncogene2004
RNA polymerase III transcription and cancer.
Review in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.
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
133 citing papers in PubMed, 1 synthesis or guideline pooled it, 207 citations in OpenAlex.
- Pooled it
- Terminator-dependent facilitated recycling of RNA polymerase III provides gene-specific transcriptional activation in vivo.Science advances · 2026Article
- Human RNA polymerase III termination favors decomposition over facilitated recycling.Nature communications · 2026Article
- Metabolism-Driven Modulation by the Human Microbiota: Implications for Cancer Therapy and Emerging Strategies.Advances in experimental medicine and biology · 2026Review
- The MTORC1 signaling pathway related gene POLR3G serves as a potential prognostic biomarker in Hepatocellular Carcinoma.Clinical and experimental medicine · 2025Article
- Maf1 cooperates with progesterone receptor to repress RNA polymerase III transcription of select tRNAs.Nucleic acids research · 2025Article
- TFIIB-related factor 2 inhibits lung squamous carcinoma cell apoptosis through SLC8A3-mediated mitochondrial homeostasis.Cell death & disease · 2025Article
- Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1-bound enhancers through interactions with the EP400 chromatin remodeler.Nucleic acids research · 2024Article
- Antitumor mechanisms and future clinical applications of the natural product triptolide.Cancer cell international · 2024Review
- Oxidative Stress, Transfer RNA Metabolism, and Protein Synthesis.Antioxidants & redox signaling · 2024Review
- RN7SL1 may be translated under oncogenic conditions.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Biallelic variants in GTF3C5, a regulator of RNA polymerase III-mediated transcription, cause a multisystem developmental disorder.Human genetics · 2024Article
- Roles of lncRNAs related to the p53 network in breast cancer progression.Frontiers in oncology · 2024Review
- "Transfer" of power: The intersection of DNA virus infection and tRNA biology.Seminars in cell & developmental biology · 2023Review
- Structural basis of TFIIIC-dependent RNA polymerase III transcription initiation.Molecular cell · 2023Article
- Selection of tRNA Genes in Human Breast Tumours Varies Substantially between Individuals.Cancers · 2023Article
- Structural basis of TFIIIC-dependent RNA Polymerase III transcription initiation.bioRxiv : the preprint server for biology · 2023Article
- nc886, an RNA Polymerase III-Transcribed Noncoding RNA Whose Expression Is Dynamic and Regulated by Intriguing Mechanisms.International journal of molecular sciences · 2023Review
- BDP1 as a biomarker in serous ovarian cancer.Cancer medicine · 2023Article
- RNA Polymerases I and III in development and disease.Seminars in cell & developmental biology · 2023Review
73 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA polymerase (pol) III synthesizes a range of essential products, including tRNA, 5S rRNA and 7SL RNA, which are required for protein synthesis and trafficking. High rates of pol III transcription are necessary for cells to sustain growth. A wide range of transformed and tumour cell types have been shown to express elevated levels of pol III products. This review will summarize what is known about the mechanisms responsible for this deregulation. Some transforming agents have been shown to stimulate expression of the pol III-specific transcription factors TFIIIB or TFIIIC2. In addition, TFIIIB is bound and activated by several oncogenic proteins, including c-Myc. Conversely, TFIIIB interacts in healthy cells with the tumour suppressors RB and p53. Indeed, the ability to limit pol III transcription through TFIIIB may contribute to their growth-suppression capacities. The function of p53 and/or RB is compromised in most if not all transformed cells; the resultant derepression of TFIIIB may provide an almost universal route to deregulate pol III transcription in cancers. In addition to effects on protein synthesis and growth, there is a precedent for a pol III product having oncogenic activity.
Indexed as
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.