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- W4289261207 abstract "The epidermal growth factor receptor (EGFR) is a prime oncogene that is frequently amplified in glioblastomas. Here we demonstrate a new tumour-suppressive function of EGFR in EGFR-amplified glioblastomas regulated by EGFR ligands. Constitutive EGFR signalling promotes invasion via activation of a TAB1–TAK1–NF-κB–EMP1 pathway, resulting in large tumours and decreased survival in orthotopic models. Ligand-activated EGFR promotes proliferation and surprisingly suppresses invasion by upregulating BIN3, which inhibits a DOCK7-regulated Rho GTPase pathway, resulting in small hyperproliferating non-invasive tumours and improved survival. Data from The Cancer Genome Atlas reveal that in EGFR-amplified glioblastomas, a low level of EGFR ligands confers a worse prognosis, whereas a high level of EGFR ligands confers an improved prognosis. Thus, increased EGFR ligand levels shift the role of EGFR from oncogene to tumour suppressor in EGFR-amplified glioblastomas by suppressing invasion. The tumour-suppressive function of EGFR can be activated therapeutically using tofacitinib, which suppresses invasion by increasing EGFR ligand levels and upregulating BIN3. Guo et al. show that ligand-induced EGFR activation suppresses invasion by upregulating BIN3 and inhibiting DOCK7-regulated Rho GTPase activity in EGFR-amplified glioblastoma, which is in contrast to the known oncogenic role for EGFR signalling." @default.
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- W4289261207 date "2022-08-01" @default.
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- W4289261207 title "EGFR ligand shifts the role of EGFR from oncogene to tumour suppressor in EGFR-amplified glioblastoma by suppressing invasion through BIN3 upregulation" @default.
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- W4289261207 cites W1975151320 @default.
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- W4289261207 cites W1998670627 @default.
- W4289261207 cites W2002832232 @default.
- W4289261207 cites W2007210314 @default.
- W4289261207 cites W2010030578 @default.
- W4289261207 cites W2014881369 @default.
- W4289261207 cites W2015814220 @default.
- W4289261207 cites W2016097940 @default.
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- W4289261207 cites W2018671779 @default.
- W4289261207 cites W2019226300 @default.
- W4289261207 cites W2019787798 @default.
- W4289261207 cites W2037720820 @default.
- W4289261207 cites W2042361125 @default.
- W4289261207 cites W2048043668 @default.
- W4289261207 cites W2054153896 @default.
- W4289261207 cites W2054727624 @default.
- W4289261207 cites W2059581116 @default.
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- W4289261207 cites W2080368097 @default.
- W4289261207 cites W2083063806 @default.
- W4289261207 cites W2086121306 @default.
- W4289261207 cites W2090826582 @default.
- W4289261207 cites W2095472784 @default.
- W4289261207 cites W2099885230 @default.
- W4289261207 cites W2100553819 @default.
- W4289261207 cites W2102626211 @default.
- W4289261207 cites W2103744931 @default.
- W4289261207 cites W2107078481 @default.
- W4289261207 cites W2108894720 @default.
- W4289261207 cites W2121625674 @default.
- W4289261207 cites W2124157901 @default.
- W4289261207 cites W2133037949 @default.
- W4289261207 cites W2136734008 @default.
- W4289261207 cites W2154391976 @default.
- W4289261207 cites W2154554776 @default.
- W4289261207 cites W2161289668 @default.
- W4289261207 cites W2161893982 @default.
- W4289261207 cites W2169039713 @default.
- W4289261207 cites W2170748325 @default.
- W4289261207 cites W2171338578 @default.
- W4289261207 cites W2218048464 @default.
- W4289261207 cites W2318368210 @default.
- W4289261207 cites W2330657714 @default.
- W4289261207 cites W2344575109 @default.
- W4289261207 cites W2416002407 @default.
- W4289261207 cites W2416369577 @default.
- W4289261207 cites W2511292374 @default.
- W4289261207 cites W2574053101 @default.
- W4289261207 cites W2613083354 @default.
- W4289261207 cites W2626445265 @default.
- W4289261207 cites W2766102202 @default.
- W4289261207 cites W2769408674 @default.
- W4289261207 cites W2783146090 @default.
- W4289261207 cites W2800726265 @default.
- W4289261207 cites W2924509582 @default.
- W4289261207 cites W2966820070 @default.
- W4289261207 cites W2981732542 @default.