ArticleNature communications2023
Elevated pre-mRNA 3' end processing activity in cancer cells renders vulnerability to inhibition of cleavage and polyadenylation.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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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.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- TENT5A Maintains MYC mRNA Stability to Enhance Osteosarcoma Stemness.Cancer research · 2026Article
- Regulation of gene expression by alternative polyadenylation in health and disease.Nature reviews. Genetics · 2026Review
- NELF prevents transcriptional readthrough into DNA replication zones in cancer cells.EMBO reports · 2026Article
- Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib.Science advances · 2026Article
- CRISPR/Cas9 screening with destabilized bicistronic fluorescent protein reporter revealed PABPN1 as a hub of regulators for alternative polyadenylation.Nucleic acids research · 2026Article
- A Unique Chimeric RNA: ERCC1-iASPP Drives Benzo[a]pyrene-Induced Lung Carcinogenesis via Dual Coding and Non-Coding Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Global mRNA 3'UTR lengthening in small-cell neuroendocrine carcinoma.bioRxiv : the preprint server for biology · 2026Article
- Transcription termination counteracts DNA damage after WEE1 inhibition.Nucleic acids research · 2026Article
- Targeting CPSF73, the mRNA 3' end processing endonuclease, moves cancer cells away from the mesenchymal state.Frontiers in immunology · 2026Article
- Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib.bioRxiv : the preprint server for biology · 2025Article
- Loss of CFIm activates YAP/TAZ and connects mRNA cleavage and polyadenylation inhibition to BRCAness.bioRxiv : the preprint server for biology · 2025Article
- Characterization and molecular targeting of CFIm25 (NUDT21/CPSF5) mRNA using miRNAs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells.Cell reports · 2025Article
- Fateful Decisions of Where to Cut the Line: Pathology Associated with Aberrant 3' End Processing and Transcription Termination.Journal of molecular biology · 2025Review
- Modulation of diverse biological processes by CPSF, the master regulator of mRNA 3' ends.RNA (New York, N.Y.) · 2024Review
- Cleavage and polyadenylation machinery as a novel targetable vulnerability for human cancer.Cancer gene therapy · 2024Article
- Splicing targeting drugs highlight intron retention as an actionable vulnerability in advanced prostate cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- CPSF3 inhibition blocks pancreatic cancer cell proliferation through disruption of core histone mRNA processing.RNA (New York, N.Y.) · 2024Article
- The anticancer compound JTE-607 reveals hidden sequence specificity of the mRNA 3' processing machinery.Nature structural & molecular biology · 2023Article
- The Advances in Deep Learning Modeling of Polyadenylation Codes.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cleavage and polyadenylation (CPA) is responsible for 3' end processing of eukaryotic poly(A)+ RNAs and preludes transcriptional termination. JTE-607, which targets CPSF-73, is the first known CPA inhibitor (CPAi) in mammalian cells. Here we show that JTE-607 perturbs gene expression through both transcriptional readthrough and alternative polyadenylation (APA). Sensitive genes are associated with features similar to those previously identified for PCF11 knockdown, underscoring a unified transcriptomic signature of CPAi. The degree of inhibition of an APA site by JTE-607 correlates with its usage level and, consistently, cells with elevated CPA activities, such as those with induced overexpression of FIP1, display greater transcriptomic disturbances when treated with JTE-607. Moreover, JTE-607 causes S phase crisis and is hence synergistic with inhibitors of DNA damage repair pathways. Together, our data reveal CPA activity and proliferation rate as determinants of CPAi-mediated cell death, raising the possibility of using CPAi as an adjunct therapy to suppress certain cancers.
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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 Socratic graph.