ArticleCell death and differentiation2013
ATM kinase enables the functional axis of YAP, PML and p53 to ameliorate loss of Werner protein-mediated oncogenic senescence.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- Proteomic profiling identifies a stromal TGF-β1/podoplanin axis as a driver of colorectal cancer progression.Journal of experimental & clinical cancer research : CR · 2025Article
- Substrate stiffness dictates unique doxorubicin-induced senescence-associated secretory phenotypes and transcriptomic signatures in human pulmonary fibroblasts.GeroScience · 2025Article
- NOTCH1 inhibition enhances immunogenicity and sensitizes triple-negative breast cancer to immune checkpoint inhibitors.Breast cancer research : BCR · 2025Article
- ATM and p53 in aging and cancer: a double-edged sword in genomic integrity.Biogerontology · 2025Review
- Substrate Stiffness Dictates Unique Doxorubicin-induced Senescence-associated Secretory Phenotypes and Transcriptomic Signatures in Human Pulmonary Fibroblasts.bioRxiv : the preprint server for biology · 2024Article
- SNORD88B-mediated WRN nucleolar trafficking drives self-renewal in liver cancer initiating cells and hepatocarcinogenesis.Nature communications · 2024Article
- Divergent roles of the Hippo pathway in the pathogenesis of idiopathic pulmonary fibrosis: tissue homeostasis and fibrosis.Inflammation and regeneration · 2023Review
- YAP Inhibition Alleviates Simulated Microgravity-Induced Mesenchymal Stem Cell Senescence via Targeting Mitochondrial Dysfunction.Antioxidants (Basel, Switzerland) · 2023Article
- Senescence induces fundamental changes in the secretome of mesenchymal stromal cells (MSCs): implications for the therapeutic use of MSCs and their derivates.Frontiers in bioengineering and biotechnology · 2023Review
- Senotherapeutics and Their Molecular Mechanism for Improving Aging.Biomolecules & therapeutics · 2022Review
- Article
- Review
- LINCing Senescence and Nuclear Envelope Changes.Cells · 2022Review
- PCAF Accelerates Vascular Senescence via the Hippo Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
- Epithelial cell transforming 2 is regulated by Yes-associated protein 1 and mediates pancreatic cancer progression and metastasis.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- YAP accelerates vascular senescence via blocking autophagic flux and activating mTOR.Journal of cellular and molecular medicine · 2021Article
- β-elemene promotes the senescence of glioma cells through regulating YAP-CDK6 signaling.American journal of cancer research · 2021Article
- The Contribution of Physiological and Accelerated Aging to Cancer Progression Through Senescence-Induced Inflammation.Frontiers in oncology · 2021Review
- Article
- YAP1-LATS2 feedback loop dictates senescent or malignant cell fate to maintain tissue homeostasis.EMBO reports · 2019Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Werner syndrome (WS) results from dysfunction of the WRN protein, and is associated with premature aging and early death. Here we report that loss of WRN function elicits accumulation of the Yes-associated protein (YAP protein), a major effector of the Hippo tumor suppressor pathway, both experimentally and in WS-derived fibroblasts. YAP upregulation correlates with slower cell proliferation and accelerated senescence, which are partially mediated by the formation of a complex between YAP and the PML protein, whose activity promotes p53 activation. The ATM kinase is necessary for YAP and PML accumulation in WRN-depleted cells. Notably, the depletion of either YAP or PML partially impairs the induction of senescence following WRN loss. Altogether, our findings reveal that loss of WRN activity triggers the activation of an ATM-YAP-PML-p53 axis, thereby accelerating cellular senescence. The latter has features of SASP (senescence-associated secretory phenotype), whose protumorigenic properties are potentiated by YAP, PML and p53 depletion.
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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.