ArticleRNA (New York, N.Y.)2016
CFIm25 regulates glutaminase alternative terminal exon definition to modulate miR-23 function.
Article in RNA (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- The distinguished predictive value of CFIm25 in schistosomal and non-schistosomal colorectal cancer.Translational cancer research · 2026Article
- Exploring Lipid Metabolic Reprogramming: Mechanistic Insights and Implications for Tumor Radiotherapy.International journal of biological sciences · 2026Review
- WTAP-Mediated Glutaminase Splicing Bias Suppresses Ferroptosis in Hepatocellular Carcinoma.Cancer communications (London, England) · 2026Article
- Reduced Usage ofPhenomics (Cham, Switzerland) · 2025Article
- A ratiometric catalog of protein isoform shifts in the cardiac fetal gene program.JCI insight · 2025Article
- Fueling Prostate Cancer: The Central Role of Glutamine/Glutamate Metabolic Reprogramming.Asian Pacific journal of cancer prevention : APJCP · 2025Review
- 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
- Involvement of oncomiRs miR-23, miR-24, and miR-27 in the regulation of alternative polyadenylation in glioblastoma via CFIm25 cleavage factor.Metabolic brain disease · 2024Article
- HuR controls glutaminase RNA metabolism.Nature communications · 2024Article
- Article
- Macrophage differentiation is marked by increased abundance of the mRNA 3' end processing machinery, altered poly(A) site usage, and sensitivity to the level of CstF64.Frontiers in immunology · 2023Article
- Impacts and mechanisms of alternative mRNA splicing in cancer metabolism, immune response, and therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Review
- Shortening of the KHDRBS1 3'UTR by alternative cleavage and polyadenylation alters miRNA-mediated regulation and promotes gastric cancer progression.American journal of translational research · 2022Article
- Cleavage factor Im 25 as a potential biomarker for prognosis of colorectal cancer.Translational cancer research · 2021Article
- Dynamic Variations of 3'UTR Length Reprogram the mRNA Regulatory Landscape.Biomedicines · 2021Review
- A glutaminase isoform switch drives therapeutic resistance and disease progression of prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Effective tools for RNA-derived therapeutics: siRNA interference or miRNA mimicry.Theranostics · 2021Review
- The role of alternative splicing in human cancer progression.American journal of cancer research · 2021Review
- Suppression of CPSF6 Enhances Apoptosis Through Alternative Polyadenylation-Mediated Shortening of theFrontiers in genetics · 2021Article
- Alternative Polyadenylation: a new frontier in post transcriptional regulation.Biomarker research · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Alternative polyadenylation (APA) and alternative splicing (AS) provide mRNAs with the means to avoid microRNA repression through selective shortening or differential usage of 3'UTRs. The two glutaminase (GLS) mRNA isoforms, termed KGA and GAC, contain distinct 3'UTRs with the KGA isoform subject to repression by miR-23. We show that depletion of the APA regulator CFIm25 causes a strong shift to the usage of a proximal poly(A) site within the KGA 3'UTR and also alters splicing to favor exclusion of the GAC 3'UTR. Surprisingly, we observe that while miR-23 is capable of down-regulating the shortened KGA 3'UTR, it has only minor impact on the full-length KGA 3'UTR, demonstrating that additional potent negative regulation of GLS expression exists beyond this single microRNA targeting site. Finally, we show that the apoptosis induced upon down-regulation of the GAC isoform can be alleviated through concurrent reduction in CFIm25 expression, revealing the sensitivity of glutaminase expression to the levels of RNA processing factors. These results exemplify the complex interplay between RNA processing and microRNA repression in controlling glutamine metabolism in cancer cells.
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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 OpenQuestion graph.