ArticleNature communications2022
A cancer-associated RNA polymerase III identity drives robust transcription and expression of snaR-A noncoding RNA.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 27 citations in OpenAlex.
- Mapping the interactome of human tRNA methyltransferase TRMT1 using dual proximity labeling.bioRxiv : the preprint server for biology · 2026Article
- Vulnerability of SRSF2-mutated chronic myelomonocytic leukemia to perturbation of the cGAS-STING pathway.Blood advances · 2026Article
- Cancer-associated snaR-A noncoding RNA interacts with core splicing machinery and disrupts processing of mRNA subpopulations.Nature communications · 2025Article
- DUSP11 is an Intracellular Innate Immune Checkpoint in Lung Adenocarcinoma.Cancer immunology research · 2025Article
- Maf1 cooperates with progesterone receptor to repress RNA polymerase III transcription of select tRNAs.Nucleic acids research · 2025Article
- Cancer-associated fibroblasts-secreted lactate promotes RNA polymerase III subunit G-mediated epithelial-mesenchymal transition in non-small cell lung cancer by increasing m6A modification of zinc finger protein 384.Journal of cell communication and signaling · 2025Article
- An RNA polymerase III tissue and tumor atlas uncovers context-specific activities linked to 3D epigenome regulatory mechanisms.bioRxiv : the preprint server for biology · 2025Article
- RNA Polymerase III-Transcribed RNAs in Health and Disease: Mechanisms, Dysfunction, and Future Directions.International journal of molecular sciences · 2025Review
- Article
- CRISPuRe-seq: pooled screening of barcoded ribonucleoprotein reporters reveals regulation of RNA polymerase III transcription by the integrated stress response via mTOR.Nucleic acids research · 2025Article
- Evidence of RNA polymerase III recruitment and transcription at protein-coding gene promoters.Molecular cell · 2024Article
- The subcellular distribution of miRNA isoforms, tRNA-derived fragments, and rRNA-derived fragments depends on nucleotide sequence and cell type.BMC biology · 2024Article
- Evidence of RNA polymerase III recruitment and transcription at protein-coding gene promoters.bioRxiv : the preprint server for biology · 2024Article
- Crosstalk between vault RNAs and innate immunity.Molecular biology reports · 2024Review
- AbioRxiv : the preprint server for biology · 2024Article
- Regulation of bacterial gene expression by non-coding RNA: It is all about time!Cell chemical biology · 2024Review
- A Combinatorial Regulatory Platform Determines Expression of RNA Polymerase III Subunit RPC7α (Cancers · 2023Article
- Regulating POLR3G by MicroRNA-26a-5p as a promising therapeutic target of lung cancer stemness and chemosensitivity.Non-coding RNA research · 2023Article
- Selection of tRNA Genes in Human Breast Tumours Varies Substantially between Individuals.Cancers · 2023Article
- Review
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
RNA polymerase III (Pol III) includes two alternate isoforms, defined by mutually exclusive incorporation of subunit POLR3G (RPC7α) or POLR3GL (RPC7β), in mammals. The contributions of POLR3G and POLR3GL to transcription potential has remained poorly defined. Here, we discover that loss of subunit POLR3G is accompanied by a restricted repertoire of genes transcribed by Pol III. Particularly sensitive is snaR-A, a small noncoding RNA implicated in cancer proliferation and metastasis. Analysis of Pol III isoform biases and downstream chromatin features identifies loss of POLR3G and snaR-A during differentiation, and conversely, re-establishment of POLR3G gene expression and SNAR-A gene features in cancer contexts. Our results support a model in which Pol III identity functions as an important transcriptional regulatory mechanism. Upregulation of POLR3G, which is driven by MYC, identifies a subgroup of patients with unfavorable survival outcomes in specific cancers, further implicating the POLR3G-enhanced transcription repertoire as a potential disease factor.
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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.