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Mutated EGFR activates AKT. 36 / 36
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"EGFR mutants promote tumorigenesis of NSCLC by constitutively activating downstream signaling effectors, including PI3K/AKT, RAS/ERK, and others.30, 31 Activated AKT, as a key downstream effector of the EGFR pathway, has been reported to activate NF‐κB and thereby regulate PD‐L1 expression."
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"As the above results demonstrate an important role for SRC, we considered if dual SRC inhibition in conjunction with inhibition of mutant EGFR driven AKT signaling could be effective in cells with EGFR gatekeeper mutations."
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"EGFR mutations activated Akt, ERK, and STAT3 to promote cell survival."
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"EGFR mutations enable constitutive activation of ERK, AKT and JAK signaling pathways, and promote tumor proliferation by inducing uncontrolled cell division and evasion of apoptosis [ 33 , 34 ]."
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"XREF_BIBR The results showed that mutant EGFR selectively activated Akt and signal transducer and activator of transcription (STAT) signaling is related to cell survival; however, mutant EGFR could not act on extracellular signal regulated kinase signaling, the function of which is to induce proliferation."
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"Mutant EGFR tumors can activate the PI3K/AKT pathway, promoting cell survival via the activation of ErbB3 [159]."
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"For example, certain mutations of epidermal growth factor receptor (EGFR) extracellular and kinase domains lead to downstream overactivation of signaling pathways, such as Ras–mitogen activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), which play a major role in cell proliferation and survival [8,9]."
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"Mutation of the EGFR tyrosine kinase domain activates the AKT pathway, resulting in tumor growth and invasion in NSCLC [268]."
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"As an initial test system for this hypothesis, we used the NSCLC line H3255, which expresses HER3, HER2, and a mutant EGFR that cooperates with HER3 to activate PI3K and Akt and is not known to express HER4 (supplemental Fig."
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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 activate ERK, AKT and STAT3 directly or through IL-6-JAK2 [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"EGFR mutations aberrantly activate its downstream proteins PI3K/AKT pathway and Erk pathway, playing an important role in the progression of NSCLC [26]."
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"Based on these results, we propose that mutant EGFR activates the PI3K and AKT pathway through both ERBB3 dependent and ERBB3 independent mechanisms."
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"Furthermore, both ALK-rearrangement and mutant EGFR upregulate PD-L1 by activating PI3K-AKT and MEK-ERK signaling pathways such constituting a direct link between oncogenic drivers and PD-L1 expression in NSCLC [84]."
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"EGFR mutations can lead to abnormal activation of EGFR, resulting in abnormal activation of Akt and STAT3/5 downstream of the EGFR signaling pathway, thereby significantly inhibiting apoptosis induction [27, 28]."
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"Of these genes, we found a coincidence of an AKT2 mutation in a lung adenocarcinoma, suggesting that alterations in the AKT signaling by both AKT2 and EGFR mutation can occur and could possibly contri[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"These results suggest that these constitutively active EGFR mutants down regulate pERK1/2 but do not activate Akt."
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"Sordella and colleagues showed that these EGFR mutants selectively activate the Akt survival pathway."
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"XREF_BIBR Consistent with these findings, pre-clinical studies have shown that those EGFR mutations that sensitize to gefitinib selectively activated the Akt pathway."
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"Because mutant EGFR potently stimulates the AKT pathway [XREF_BIBR], we anticipated that a similar mechanism of BIM induction would be activated after gefitinib treatment of NSCLC cells expressing hyperactive mutant EGFR."
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"15 Mutant EGFR, such as exon 19 deletions and L858R, activate Akt and STAT signaling pathways, which protect cells against apoptosis and promote cell survival."
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"EGFRvIII is a constitutively active EGFR mutant that persistently activates the PI3K-Akt signaling compared with the WT EGFR."
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"43 In non-small cell lung cancer (NSCLC), EGFR mutations promote proliferation, inhibit apoptosis and migration, and then promote tumor progression by activating the PI3K/AKT and JAK/STAT signaling pathways.44 Therefore, EGFR and the JAK/STAT and PI3K/Akt signaling pathways are closely related."
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"Gefitinib induced substantial clinical responses and reduced tumour burden in ~ 10% of patients with chemotherapy-refractory non small cell lung cancers; however, the majority of these patients had EGFR mutations that constitutively activated the antiapoptotic protein AKT (Baselga, 2002; Fukuoka et al, 2003; Kris et al, 2003; Giaccone et al, 2004)."
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"Mutations of the epidermal growth factor receptor (EGFR) selectively activate Akt and signal transducer and activator of transcription (STAT) pathways that are important in lung cancer cell survival."
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"Akt pathway activation by mutant EGFR is mediated by HER3 coupled to PI3K, which is read-Figure 1."
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"Mutant EGFR expressing cells, such as HCC827, selectively activate Akt and signal transducer and activator of transcription (STAT) pathway which promote cell survival, whereas wild-type EGFR expressin[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Our findings that both EML4-ALK and mutant EGFR upregulate PD-L1 by activating PI3K-AKT and MEK-ERK signaling pathways in NSCLC reveal a direct link between oncogenic drivers and PD-L1 expression."
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"XREF_BIBR - XREF_BIBR Mutant EGFR heterodimerizes with ErbB-3 to activate the PI3K and Akt signaling pathway."
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"It is also known that EGFR mutations activated the antiapoptotic protein Akt (Sordella et al, 2004), and that patients whose tumours have activated Akt are more sensitive to TKIs than patient whose tumours are phospho-AKT negative (Cappuzzo et al, 2004)."
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"EGFR mutations activate mitogen activated protein kinase (MAPK) / extracellular signal regulated kinase 1/2 (ERK1/2) and phosphatidylinositol 3 ' -kinase-AKT (PI3K and AKT) pro survival pathways."
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"Mutant EGFR upregulated PD-L1 by activating PI3K-AKT and MEK-ERK signaling pathways in NSCLC."
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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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"XREF_BIBR - XREF_BIBR Mutant EGFR leads to constitutive activation of downstream ERK, PI3K and Akt, and STAT signalling resulting in ' oncogene addiction ' and tumour cell growth and survival."
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"Mutant EGFR is reported to selectively activate Akt and signal transducer and activator of transcription protein (STAT) signaling pathways that promote cell survival but less effect on the mitogen act[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Mechanistically, EGFR mutation constitutively activated downstream ERK and AKT pathways to respectively upregulate the transcriptional factors c-Myc and NFκB, both of which structurally bound to the promotor region of CD47 and actively transcribed this "don't eat me" signal."
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