ArticleNature communications2013
Prelamin A causes progeria through cell-extrinsic mechanisms and prevents cancer invasion.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Mechanosensing by the nucleus: From pathways to scaling relationships.The Journal of cell biology · 2017Pooled it
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- Murine Progeria Model Exhibits Delayed Fracture Healing With Senescent Phenotype and Dysregulated Immune Response.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- Homoharringtonine exhibits senotherapeutic activity that mitigates diet- and age-associated obesity and insulin resistance and extends lifespan in mice.Nature communications · 2026Article
- Progerin regulates actin cytoskeletal remodeling and inhibits EMT and metastasis in triple‑negative breast cancer cells.International journal of oncology · 2025Article
- Immune system development-related signature predicts prognosis and sorafenib-treatment resistance of hepatocellular carcinoma by intergrating machine learning and single-cell analyses.Scientific reports · 2025Article
- Disease pathogenicity in Hutchinson-Gilford progeria syndrome mice: insights from lung-associated alterations.Molecular medicine (Cambridge, Mass.) · 2025Article
- Progerin Inhibits the Proliferation and Migration of Melanoma Cells by Regulating the Expression of Paxillin.OncoTargets and therapy · 2024Article
- The secretome atlas of two mouse models of progeria.Aging cell · 2023Article
- Extracellular Matrix Dynamics as an Emerging yet Understudied Hallmark of Aging and Longevity.Aging and disease · 2023Review
- Construction and validation of an aging-related gene signature for prognosis prediction of patients with breast cancer.Cancer reports (Hoboken, N.J.) · 2023Article
- Impact of aging on tendon homeostasis, tendinopathy development, and impaired healing.Connective tissue research · 2023Review
- LINCing Senescence and Nuclear Envelope Changes.Cells · 2022Review
- Lamin A and the LINC complex act as potential tumor suppressors in Ewing Sarcoma.Cell death & disease · 2022Article
- Pharmacotherapy to gene editing: potential therapeutic approaches for Hutchinson-Gilford progeria syndrome.GeroScience · 2020Review
- Article
- Overexpression of Progerin Results in Impaired Proliferation and Invasion of Non-Small Cell Lung Cancer Cells.OncoTargets and therapy · 2020Article
- The Role of Matrix Metalloproteinases (MMP-2 and MMP-9) in Ageing and Longevity: Focus on Sicilian Long-Living Individuals (LLIs).Mediators of inflammation · 2020Article
- Progeria: A Rare Genetic Syndrome.Indian journal of clinical biochemistry : IJCB · 2020Review
- Differential proteomics mass spectrometry of melanosis coli.American journal of translational research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Defining the relationship between ageing and cancer is a crucial but challenging task. Mice deficient in Zmpste24, a metalloproteinase mutated in human progeria and involved in nuclear prelamin A maturation, recapitulate multiple features of ageing. However, their short lifespan and serious cell-intrinsic and cell-extrinsic alterations restrict the application and interpretation of carcinogenesis protocols. Here we present Zmpste24 mosaic mice that lack these limitations. Zmpste24 mosaic mice develop normally and keep similar proportions of Zmpste24-deficient (prelamin A-accumulating) and Zmpste24-proficient (mature lamin A-containing) cells throughout life, revealing that cell-extrinsic mechanisms are preeminent for progeria development. Moreover, prelamin A accumulation does not impair tumour initiation and growth, but it decreases the incidence of infiltrating oral carcinomas. Accordingly, silencing of ZMPSTE24 reduces human cancer cell invasiveness. Our results support the potential of cell-based and systemic therapies for progeria and highlight ZMPSTE24 as a new anticancer target.
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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.