ArticleCancer cell2018
PTBP1-Mediated Alternative Splicing Regulates the Inflammatory Secretome and the Pro-tumorigenic Effects of Senescent Cells.
Open access · hybridAbstract read
In one paragraph
Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.
0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed
13.8field-weighted citation impact, top 1% of its field
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
154 citing papers in PubMed, 244 citations in OpenAlex.
- The crosstalk between alternative splicing and histone ubiquitination modulates fast chemical reprogramming to pluripotency.Stem cell reports · 2026Article
- Alternative Splicing Constitutes a Transcription-independent Regulatory Layer in Replicative Senescence of Human Umbilical Cord Mesenchymal Stem Cells.Stem cell reviews and reports · 2026Article
- RAISE quantifies RNA binding protein activity via transcriptomic profiling.Nature communications · 2026Article
- Deconvoluting the multi-faceted roles of alternative splicing events in cancer: From underlying mechanisms to innovative therapeutics.Acta pharmaceutica Sinica. B · 2026Review
- SenFlag gene signature identifies senescent cells in mouse and human tissues through a conserved core transcriptional program.The EMBO journal · 2026Article
- METTL3 regulates exocytosis independently of mScience advances · 2026Article
- Spliceosome induction is a druggable dependency of RAS-driven senescence and cancer.Nature communications · 2026Article
- Exocyst complex regulates fungal-mediated IL-33 release from cancer cells.Signal transduction and targeted therapy · 2026Article
- CUL5 E3 ubiquitin ligase regulates the evasion of bladder cancer cells to CD8+ T cell-mediated killing by inhibiting autophagy.PLoS biology · 2026Article
- PTBP1-mediated inhibition of circular RNA SCMH1 biogenesis impairs brain recovery after ischemic stroke.Theranostics · 2026Article
- The paradox of cellular senescence in prostate cancer: from tumor suppression to tumor promotion.Frontiers in oncology · 2026Review
- Research progress on the spatiotemporal dynamics of therapy-induced senescence in remodeling the tumor microenvironment.Frontiers in immunology · 2026Review
- Review
- Long Non-Coding RNA IGFRIL Couples with PTBP1 to Destabilize IGFBP3 mRNA to Promote the IGF1R-AKT-mTOR Axis and Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Transcriptomic analysis reveals lung cancer and subtype-specific alternative splicing biomarkers regulated by RNA-binding proteins.Molecular therapy. Nucleic acids · 2025Article
- The states of senescent cells.Biochemical Society transactions · 2025Review
- Depletion of Polypyrimidine tract binding protein 1 (ptbp1) activates Müller glia-derived proliferation during zebrafish retina regeneration via modulation of the senescence secretome.Experimental eye research · 2025Article
- PTBP1 and Cancer: From RNA Regulation to Therapeutic Potential.Journal of cellular and molecular medicine · 2025Review
- Review
- Targeting PTBP3-Mediated Alternative Splicing of COX11 Induces Cuproptosis for Inhibiting Gastric Cancer Peritoneal Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
94 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
23 authors at 12 institutions in 5 countries.
Athena GeorgilisMRC London Institute of Medical Sciences (LMS), Du Cane Road, London W12 0NN, UK; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Sabrina KlotzDepartment of Internal Medicine VIII, University Hospital Tübingen, Tübingen 72076, Germany; Department of Physiology I, Institute of Physiology, Eberhard Karls University Tübingen, Tübingen 72076, Germany.
Christopher J HanleyCancer Sciences Unit, Cancer Research UK Centre, University of Southampton, Somers Building, Southampton SO16 6YD, UK.
Nicolas HerranzMRC London Institute of Medical Sciences (LMS), Du Cane Road, London W12 0NN, UK; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Benedikt WeirichDivision of Chronic Inflammation and Cancer, German Cancer Research Centre (DKFZ), Heidelberg 69121, Germany.
Beatriz MoranchoPreclinical Research Program, Vall d'Hebron Institute of Oncology (VHIO) and CIBERONC, Barcelona 08035, Spain.
Ana Carolina LeoteInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal.
Luana D'ArtistaDepartment of Internal Medicine VIII, University Hospital Tübingen, Tübingen 72076, Germany; Department of Physiology I, Institute of Physiology, Eberhard Karls University Tübingen, Tübingen 72076, Germany.
Suchira GallageMRC London Institute of Medical Sciences (LMS), Du Cane Road, London W12 0NN, UK; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK; Division of Chronic Inflammation and Cancer, German Cancer Research Centre (DKFZ), Heidelberg 69121, Germany.
Marco SeehawerDepartment of Internal Medicine VIII, University Hospital Tübingen, Tübingen 72076, Germany; Department of Physiology I, Institute of Physiology, Eberhard Karls University Tübingen, Tübingen 72076, Germany.
Thomas CarrollMRC London Institute of Medical Sciences (LMS), Du Cane Road, London W12 0NN, UK; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Gopuraja DharmalingamMRC London Institute of Medical Sciences (LMS), Du Cane Road, London W12 0NN, UK; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Keng Boon WeeInstitute of High Performance Computing, A(∗)STAR, 1 Fusionopolis Way, #16-16 Connexis, Singapore 138632, Singapore; Bioinformatics Institute, A(∗)STAR, 30 Biopolis Street, #07-01 Matrix, Singapore 138671, Singapore.
Marco MelloneCancer Sciences Unit, Cancer Research UK Centre, University of Southampton, Somers Building, Southampton SO16 6YD, UK.
Joaquim PomboMRC London Institute of Medical Sciences (LMS), Du Cane Road, London W12 0NN, UK; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Danijela HeideDivision of Chronic Inflammation and Cancer, German Cancer Research Centre (DKFZ), Heidelberg 69121, Germany.
Ernesto GuccioneMethyltransferases in Development and Disease Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A(∗)STAR), Singapore, Singapore.
Joaquín ArribasPreclinical Research Program, Vall d'Hebron Institute of Oncology (VHIO) and CIBERONC, Barcelona 08035, Spain; Department of Biochemistry and Molecular Biology, Universitat Autónoma de Barcelona, Campus de la UAB, Bellaterra 08193, Spain; Institució Catalana de Recerca i Estudis Avançats (ICREA), Barcelona 08010, Spain.
Nuno L Barbosa-MoraisInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal.
Mathias HeikenwalderDivision of Chronic Inflammation and Cancer, German Cancer Research Centre (DKFZ), Heidelberg 69121, Germany.
Gareth J ThomasCancer Sciences Unit, Cancer Research UK Centre, University of Southampton, Somers Building, Southampton SO16 6YD, UK.
Lars ZenderDepartment of Internal Medicine VIII, University Hospital Tübingen, Tübingen 72076, Germany; Department of Physiology I, Institute of Physiology, Eberhard Karls University Tübingen, Tübingen 72076, Germany; Translational Gastrointestinal Oncology Group, German Consortium for Translational Cancer Research (DKTK), German Cancer Research Center (DKFZ), Heidelberg 69120, Germany.
Jesús GilMRC London Institute of Medical Sciences (LMS), Du Cane Road, London W12 0NN, UK; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK. Electronic address: jesus.gil@imperial.ac.uk.
German Cancer Research Center · DEImperial College London · GBMRC London Institute of Medical Sciences · GBCancer Research UK · GBUniversity of Lisbon · PTUniversity of Tübingen · DEVall d'Hebron Institute of OncologyAgency for Science, Technology and Research · SGHeidelberg University · DEInstitute of Molecular and Cell Biology · SGUniversity Children's Hospital Tübingen · DEUniversity of Southampton · GB
Funding
Medical Research Council MC-A652-5PZ00Medical Research Council MC_U120085810
Abstract
Oncogene-induced senescence is a potent tumor-suppressive response. Paradoxically, senescence also induces an inflammatory secretome that promotes carcinogenesis and age-related pathologies. Consequently, the senescence-associated secretory phenotype (SASP) is a potential therapeutic target. Here, we describe an RNAi screen for SASP regulators. We identified 50 druggable targets whose knockdown suppresses the inflammatory secretome and differentially affects other SASP components. Among the screen candidates was PTBP1. PTBP1 regulates the alternative splicing of genes involved in intracellular trafficking, such as EXOC7, to control the SASP. Inhibition of PTBP1 prevents the pro-tumorigenic effects of the SASP and impairs immune surveillance without increasing the risk of tumorigenesis. In conclusion, our study identifies SASP inhibition as a powerful and safe therapy against inflammation-driven cancer.
Indexed as
Cellular SenescenceAlternative SplicingAnimalsCell ProliferationCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHeterogeneous-Nuclear RibonucleoproteinsHumansInflammationMCF-7 CellsMice, Inbred C57BLMice, TransgenicNeoplasmsParacrine CommunicationPhenotypeExoc7 protein, mouseHeterogeneous-Nuclear RibonucleoproteinsPolypyrimidine Tract-Binding ProteinPTBP1 protein, humanPtbp1 protein, mouseVesicular Transport Proteinsalternative splicingEXOC7Oncogene-induced senescencePTBP1RNAi screenSASPsenescence
Identifiers
What OpenQuestion holds
Textmetadata
LicenceCC BY
Read underepoch 390
Registered trials
None linked
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.