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• W2594353026 abstract "Abstract Multiple signalling events interact in cancer cells. Oncogenic Ras cooperates with Egfr, which cannot be explained by the canonical signalling paradigm. In turn, Egfr cooperates with Hedgehog signalling. How oncogenic Ras elicits and integrates Egfr and Hedgehog signals to drive overgrowth remains unclear. Using a Drosophila tumour model, we show that Egfr cooperates with oncogenic Ras via Arf6, which functions as a novel regulator of Hh signalling. Oncogenic Ras induces the expression of Egfr ligands. Egfr then signals through Arf6, which regulates Hh transport to promote Hh signalling. Blocking any step of this signalling cascade inhibits Hh signalling and correspondingly suppresses the growth of both, fly and human cancer cells harbouring oncogenic Ras mutations. These findings highlight a non-canonical Egfr signalling mechanism, centered on Arf6 as a novel regulator of Hh signalling. This explains both, the puzzling requirement of Egfr in oncogenic Ras-mediated overgrowth and the cooperation between Egfr and Hedgehog." @default.
• W2594353026 created "2017-03-16" @default.
• W2594353026 creator A5051843581 @default.
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• W2594353026 date "2017-03-10" @default.
• W2594353026 modified "2023-10-10" @default.
• W2594353026 title "EGFR/ARF6 regulation of Hh signalling stimulates oncogenic Ras tumour overgrowth" @default.
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• W2594353026 doi "https://doi.org/10.1038/ncomms14688" @default.
• W2594353026 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5353614" @default.
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• W2594353026 hasPublicationYear "2017" @default.
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