ArticleProceedings of the National Academy of Sciences of the United States of America2016
Targeting of Ras-mediated FGF signaling suppresses Pten-deficient skin tumor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Formation of benign tumors by stem cell deregulation.PLoS genetics · 2022Review
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- The role of microRNAs in diseases and related signaling pathways.Molecular biology reports · 2022Review
- Fibroblast growth factor receptor signalling dysregulation and targeting in breast cancer.Open biology · 2022Review
- Lacrimal gland budding requires PI3K-dependent suppression of EGF signaling.Science advances · 2021Article
- The Hippo pathway integrates PI3K-Akt signals with mechanical and polarity cues to control tissue growth.PLoS biology · 2019Article
- Review
- Deciphering role of FGFR signalling pathway in pancreatic cancer.Cell proliferation · 2019Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Deficiency in PTEN (phosphatase and tensin homolog deleted on chromosome 10) is the underlying cause of PTEN hamartoma tumor syndrome and a wide variety of human cancers. In skin epidermis, we have previously identified an autocrine FGF signaling induced by loss of Pten in keratinocytes. In this study, we demonstrate that skin hyperplasia requires FGF receptor adaptor protein Frs2α and tyrosine phosphatase Shp2, two upstream regulators of Ras signaling. Although the PI3-kinase regulatory subunits p85α and p85β are dispensable, the PI3-kinase catalytic subunit p110α requires interaction with Ras to promote hyperplasia in Pten-deficient skin, thus demonstrating an important cross-talk between Ras and PI3K pathways. Furthermore, genetic and pharmacological inhibition of Ras-MAPK pathway impeded epidermal hyperplasia in Pten animals. These results reveal a positive feedback loop connecting Pten and Ras pathways and suggest that FGF-activated Ras-MAPK pathway is an effective therapeutic target for preventing skin tumor induced by aberrant Pten signaling.
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