IndraLab

Statements

Mutated EGFR activates STAT3. 20 / 20
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"EGFR mutations may decrease the number of CD8+ cells, elevate the Treg population, and activate the STAT-3 intracellular pathway, leading to immune escape and increased resistance to targeted drugs (82)."
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"Greulich et al. reported that STAT3 was activated by various EGFR mutations, including the exon 19 in-frame deletion or the exon 21 L858R point mutation, and may contribute to the oncogenic effects of these mutations in fibroblasts and human lung cancer cells [XREF_BIBR]."
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"The mechanism whereby mutant EGFR drives STAT3 activation is indirect, as it requires upregulation of the cytokine IL-6, which activated the gp130 and JAK pathway [XREF_BIBR] (XREF_FIG)."
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"The mutant EGFR could activate signal transducer and activator of transcription -3 (STAT3) pathway via interleukin-6 upregulation in primary human lung cancer leading to cancer progression (Gao et al., 2007; Wang et al., 2013)."
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"For example, acylglycerol kinase potentiates JAK2 and STAT3 signaling in ESCC XREF_BIBR; Epstein-Barr virus (EBV)-encoded proteins constitutively activated STAT3 in NPC XREF_BIBR, XREF_BIBR; and, EGFR mutation mediates STAT3 activation via IL-6 production in lung cancer XREF_BIBR."
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"EGFR mutations activate ERK, AKT and STAT3 directly or through IL-6-JAK2 [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"Activation mutations of EGFR have been reported to activate STAT3, which is required for the oncogenic effects of EGFR mutations [XREF_BIBR, XREF_BIBR]."
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"NCI-H1650 is a lung adenocarcinoma cell, in which a mutant EGFR regulates the expression of the IL-6 cytokine and leads to the activation of JAK and STAT3 pathway."
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"EGFR mutations cause abnormal activation of the downstream JAK/STAT3 signalling pathway, leading to the expression of increased phosphorylated STAT3, and hence abnormal tumor proliferation, angiogenesis, invasion, and metastasis."
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"EGFR mutations activate phosphatidylinositol 3-kinase (PI3K)/AKT, Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3), but less so Ras and mitogen activated protein kinase (MAPK)."
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"EGFR mutations cause abnormal activation of the downstream JAK/STAT3 signalling pathway, leading to increased expression of phosphorylated STAT3, followed by abnormal tumor growth, angiogenesis, invasion, and metastasis."
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"Stat3 is activated by mutant EGFR and JAK, and notably, pStat3 is associated with tumor cell proliferation and angiogenesis [XREF_BIBR]."
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"EGFR mutations activate MAPK, PI3K-AKT, and STAT3 directly or through IL-6-JAK2 (5,10,21)."
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"Human lung cancer cell lines with activating EGFR mutations have shown marked STAT3 activation; however, targeting EGFR mutations can not effectively inhibit STAT3 activation."
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"Previous findings have shown that EGFR mutations activate STAT3 (55)."
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"Our results also suggest that while activating mutations of EGFR may enhance IL-6 production and autocrine stimulation of STAT3 activity, additional cellular factors are important in modulating this pathway and the response of cells to IL6."
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"Although STAT3 is activated by EGFR mutations [XREF_BIBR, XREF_BIBR], other receptor and non receptor tyrosine kinases such as the interleukin-6 (IL-6)/gp130 receptor can also stimulate STAT3 activation [XREF_BIBR]."
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"Activation of the AKT and STAT3 pathways and prolonged survival by a mutant EGFR in human lung cancer cells."
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"It was also noted that EGFR mutant lung cancer cell lines selectively activate AKT and STAT3 signaling pathways, promoting cell survival."
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"EGFR mutations activated Akt, ERK, and STAT3 to promote cell survival."
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