IndraLab

Statements

PTPN11 activates EGFR. 10 / 14
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"EGFR was moderately activated (pEGFR) by both the RAS and RAF (RAF1 S257L, RAF1 D486G, HRAS G12S) and PTPN11 (PTPN11 N308D, PTPN11 Q510E, PTPN11 Q510E) transgenes."
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"Our data suggest that the silencing of miR-489 expression, and subsequent overexpression of PTPN11, leads to abnormal EGFR signalling."
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"To our knowledge, this is the first study showing that the protein tyrosine phosphatase, SHP-2 mediates oncogenic EGFRvIII signals."
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"Additional potential mechanisms of action of 5-ASA include enhanced apoptosis via inhibition of NF-kappaB and p38 and MAP kinases, decreased Wnt and beta-catenin activity and elevation of SH-PTP-2, a phosphatase that targets and inactivates the EGF receptor [XREF_BIBR]."
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"Many studies have shown that SHP-2 is required to activate wild-type EGFR signaling pathways."
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"In this regard the phosphatase that targets ERBB1, SHP2, is different from the phosphatase that targets c-Met, receptor protein tyrosine phosphatase beta."
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"Inhibition of SHP-2 expression by Shp-2 siRNA inhibited cell growth, transformation and altered morphology of these EGFRvIII transformed GBM cells."
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"To understand the molecular mechanisms by which this oncoprotein alters transforming phenotypes, and since our previous work indicated that SHP-2 protein tyrosine phosphatase activity modulated EGFRvIII activation and downstream signaling, we examined whether SHP-2 plays a role in EGFRvIII induced oncogenesis by using both PTEN deficient U87MG.EGFRvIII and PTEN-intact LN229.EGFRvIII cells."
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"These results were also supported by the finding that quercetin decreased the expression of SHP2 and subsequently downregulated the activation of epidermal growth factor receptor (EGFR) in HeLa cervical cancer cells [XREF_BIBR]."
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"Further genetic analyses showed that a SHP-2 heterozygous mutation dominantly enhanced the phenotypes of EGF receptor weak allele (wa-2 and wa-2) toward EGF receptor null mutant mice."
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