ArticleThe Journal of clinical investigation2010
Wilms tumor 1 (WT1) regulates KRAS-driven oncogenesis and senescence in mouse and human models.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.
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Who cites it
83 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Wilms' tumor 1 (WT1) expression and prognosis in solid cancer patients: a systematic review and meta-analysis.Scientific reports · 2015Pooled it
- Wilms tumor 1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions.The Journal of clinical investigation · 2025Article
- Article
- Immunotherapy Applications for Thymine Dimers and WT1 Antigen in Renal Cancers: A Comparative Statistical Analysis.Journal of personalized medicine · 2024Article
- Wilms' tumor 1 (WT1) antigen is overexpressed in Kaposi Sarcoma and is regulated by KSHV vFLIP.PLoS pathogens · 2024Article
- Wilms' tumour gene 1 (WT1) enhances non-small cell lung cancer malignancy and is inhibited by microRNA-498-5p.BMC cancer · 2023Article
- The phospholipid transporter PITPNC1 links KRAS to MYC to prevent autophagy in lung and pancreatic cancer.Molecular cancer · 2023Article
- High prevalence of Wilms tumor 1 expression in multiple myeloma and plasmacytoma: A cohort of 142 Asian patients' samples.Pathology oncology research : POR · 2023Article
- Synthetic Vulnerabilities in the KRAS Pathway.Cancers · 2022Review
- Article
- Pharmacological or genetic inhibition of hypoxia signaling attenuates oncogenic RAS-induced cancer phenotypes.Disease models & mechanisms · 2022Article
- Akt-mediated Ephexin1-Ras interaction promotes oncogenic Ras signaling and colorectal and lung cancer cell proliferation.Cell death & disease · 2021Article
- A systematic analysis of genetic interactions and their underlying biology in childhood cancer.Communications biology · 2021Article
- Targeting KRAS: The Elephant in the Room of Epithelial Cancers.Frontiers in oncology · 2021Review
- KRAS-Mutant Non-Small Cell Lung Cancer: An Emerging Promisingly Treatable Subgroup.Frontiers in oncology · 2021Review
- The RASSF1A Tumor Suppressor Binds the RasGAP DAB2IP and Modulates RAS Activation in Lung Cancer.Cancers · 2020Article
- The effects of mutant Ras proteins on the cell signalome.Cancer metastasis reviews · 2020Review
- Wilms' tumor 1 (Cell cycle (Georgetown, Tex.) · 2020Article
- Phenotypic screening using large-scale genomic libraries to identify drug targets for the treatment of cancer.Oncology letters · 2020Review
- The Mir181ab1 cluster promotes KRAS-driven oncogenesis and progression in lung and pancreas.The Journal of clinical investigation · 2020Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 1 country.
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Abstract
KRAS is one of the most frequently mutated human oncogenes. In some settings, oncogenic KRAS can trigger cellular senescence, whereas in others it produces hyperproliferation. Elucidating the mechanisms regulating these 2 drastically distinct outcomes would help identify novel therapeutic approaches in RAS-driven cancers. Using a combination of functional genomics and mouse genetics, we identified a role for the transcription factor Wilms tumor 1 (WT1) as a critical regulator of senescence and proliferation downstream of oncogenic KRAS signaling. Deletion or suppression of Wt1 led to senescence of mouse primary cells expressing physiological levels of oncogenic Kras but had no effect on wild-type cells, and Wt1 loss decreased tumor burden in a mouse model of Kras-driven lung cancer. In human lung cancer cell lines dependent on oncogenic KRAS, WT1 loss decreased proliferation and induced senescence. Furthermore, WT1 inactivation defined a gene expression signature that was prognostic of survival only in lung cancer patients exhibiting evidence of oncogenic KRAS activation. These findings reveal an unexpected role for WT1 as a key regulator of the genetic network of oncogenic KRAS and provide important insight into the mechanisms that regulate proliferation or senescence in response to oncogenic signals.
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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.