ArticleThe Journal of clinical investigation2013
Thrombospondin-1 mediates oncogenic Ras-induced senescence in premalignant lung tumors.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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
38 citing papers in PubMed, 56 citations in OpenAlex.
- Targeting CD47-mediated cancer senescence, a novel strategy for cancer immunotherapy.Frontiers in immunology · 2026Review
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- Involvement of Matricellular Proteins in Cellular Senescence: Potential Therapeutic Targets for Age-Related Diseases.International journal of molecular sciences · 2024Review
- Phase 1 dose expansion and biomarker study assessing first-in-class tumor microenvironment modulator VT1021 in patients with advanced solid tumors.Communications medicine · 2024Article
- PP2A Affects Angiogenesis via Its Interaction with a Novel Phosphorylation Site of TSP1.International journal of molecular sciences · 2024Article
- Article
- Decellularized Colorectal Cancer Matrices as Bioactive Scaffolds for Studying Tumor-Stroma Interactions.Cancers · 2022Review
- Apatinib inhibits glioma cell malignancy in patient-derived orthotopic xenograft mouse model by targeting thrombospondin 1/myosin heavy chain 9 axis.Cell death & disease · 2021Article
- Decreased Thrombospondin-1 and Bone Morphogenetic Protein-4 Serum Levels as Potential Indices of Advanced Stage Lung Cancer.Journal of clinical medicine · 2021Article
- Extracellular Matrix Biomarkers in Colorectal Cancer.International journal of molecular sciences · 2021Review
- Functions of Thrombospondin-1 in the Tumor Microenvironment.International journal of molecular sciences · 2021Review
- SUV39H2 epigenetic silencing controls fate conversion of epidermal stem and progenitor cells.The Journal of cell biology · 2021Article
- Tumor Secretome to Adoptive Cellular Immunotherapy: Reduce Me Before I Make You My Partner.Frontiers in immunology · 2021Review
- Caveolin-1, a master regulator of cellular senescence.Cancer metastasis reviews · 2020Review
- The Role of the ECM in Lung Cancer Dormancy and Outgrowth.Frontiers in oncology · 2020Review
- Chemotherapy-induced senescence, an adaptive mechanism driving resistance and tumor heterogeneity.Cell cycle (Georgetown, Tex.) · 2019Review
- Regulation of senescence escape by TSP1 and CD47 following chemotherapy treatment.Cell death & disease · 2019Article
- RASSF1A Deficiency Enhances RAS-Driven Lung Tumorigenesis.Cancer research · 2018Article
- Caveolin-1 promotes the tumor suppressor properties of oncogene-induced cellular senescence.The Journal of biological chemistry · 2018Article
- p53 loss does not permit escape from BrafOncogene · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Progression of premalignant lesions is restrained by oncogene-induced senescence. Oncogenic Ras triggers senescence in many organs, including the lung, which exhibits high levels of the angiogenesis inhibitor thrombospondin-1 (TSP-1). The contribution of TSP-1 upregulation to the modulation of tumorigenesis in the lung is unclear. Using a mouse model of lung cancer, we have shown that TSP-1 plays a critical and cell-autonomous role in suppressing Kras-induced lung tumorigenesis independent of its antiangiogenic function. Overall survival was decreased in a Kras-driven mouse model of lung cancer on a Tsp-1-/- background. We found that oncogenic Kras-induced TSP-1 upregulation in a p53-dependent manner. TSP-1 functioned in a positive feedback loop to stabilize p53 by interacting directly with activated ERK. TSP-1 tethering of ERK in the cytoplasm promoted a level of MAPK signaling that was sufficient to sustain p53 expression and a senescence response. Our data identify TSP-1 as a p53 target that contributes to maintaining Ras-induced senescence in the lung.
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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.