IndraLab
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"Together
with our previous finding that VGF-induced EGFR activates non-canonical STAT3
phosphorylation to increase TCA cycle intermediate levels (10), these findings highlight VGF’s multiple roles in
rewiring host metabolism during VACV infection by modulating various cellular
signaling pathways and metabolic processes.VACV induces profound alterations of metabolism in its host cells including oxidative
phosphorylation (OXPHOS), the oxygen consumption rate (OCR), and the TCA cycle
metabolites (10, 12, 72, 73)."
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"Significantly, ZD6474 effectively suppressed EGFRvIII stimulated protein phosphorylation of Stat3 and Akt and protein expression of Bcl-X L in U87MG and EGFRvIII glioma cells that retained EGFRvIII expression in vitro and in vivo (XREF_FIG), whereas minimal effect was found in parental U87MG glioma cells lacking EGFRvIII (XREF_FIG)."
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"EGFR overexpression increased the phosphorylation of EGFR, Akt, and STAT3 signaling proteins and could partly restored the inhitory effect of MSA treatment, including the phosphorylation of EGFR, Akt, STAT3 (XREF_FIG) and IL-6 mRNA levels in both KYSE150 and KYSE 510 cells (XREF_FIG)."
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"Since we found that irradiation specifically suppressed STAT1 and STAT3 phosphorylation in IFNγ-treated A549 cells in this study, we speculated that STAT3 caused radioresistance was mediated by overexpression and activation of mutated EGFR in lung cancer after survived in RT treatment.Since the characteristic of autophosphrylation of EGFR exon 19 deletion, EGF did not affect STAT3 phosphorylation but IFNγ caused highly STAT3 phosphorylation in HCC827."
| PMC
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"STAT3 phosphorylation is catalyzed by various tyrosine kinases, including receptor tyrosine kinases (RTKs) with intrinsic enzyme activity, such as vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), colony-stimulating factor-1 receptor (CSF1R), and epidermal growth factor receptor (EGFR) [38]."
sparser
"Curcumin ( xref ) is known to inhibit STAT3 phosphorylation by EGFR, Src, and Jak2, the upstream kinases responsible for activation of STAT3 whereas AG490 ( xref ) is a specific inhibitor of Jak2 kinase which is primarily responsible for STAT3 phosphorylation through IL-6 receptor."
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"EGFR-mutant proteins, especially T790M mutant, bind to phosphorylated β-catenin and are reportedly stabilized by EGFR TKI treatment.38 39 STAT3, located downstream of NOTCH signaling, is also phosphorylated by EGFR TKI treatment,40 which induces a stem cell-like phenotype or epithelial-to-mesenchymal transition phenotype."
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"In lung adenocarcinoma, CINDy specifically highlights modulatory interactions that affect epithelial proliferation, such as the direct phosphorylation by the Epidermal Growth Factor Receptor (EGFR) of the STAT1 XREF_BIBR and STAT3 XREF_BIBR TFs, a fundamental and well established step in the proliferative signal transduction cascade that was not detected by MINDy."
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"In one study, using lung carcinoma cell line, EGFR inhibition did not block STAT3 phosphorylation and growth arrest, suggesting that upstream pathways, such as JAK and IL6 receptor, may play a role in activating STAT3 and contributing to oncogenesis in lung tumors, even with EGFR activation [XREF_BIBR]."
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"The mechanism may be that inhibition of core fucosylation of the EGF receptor inactivates the EGF signaling pathway by suppressing the phosphorylation of STAT3 and NF-κB in the peritoneal membrane of rats with peritoneal fibrosis, although further investigation is required.Figure 1."
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"This fact, along with using only one method to analyze the EVs, could be seen as a limitation of the study.Finally, we have relied on the published evidence, and have not investigated the possible expression of EGFR and other receptors, which may promote the aberrant regulation of STAT3 phosphorylation in the cases in our study."
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"In other studies, cells were treated with various specific pharmacological inhibitors where phosphorylation of Stat3 was not reduced by epidermal growth factor receptor and Mitogen activated protein and extracellular signal regulate kinase kinase (MEK1/2) inhibitors, suggesting lack of significant roles of these in Stat3 activation in DU145 cells."
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"Western blots confirmed decreased pJAK2, total JAK2 (tJAK2) and pSTAT3 in NPcis; Wa2/+ mouse GEM-PNST tumors compared to the NPcis GEM-PNSTs (XREF_FIG), suggesting that the decrease of pSTAT3 (Tyr 705) is attributed at least in part JAK2, but we can not exclude the possibility that the STAT3 is directly phosphorylated and activated by EGFR."
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"Consequently, the inhibition of EGFR by bufalin in FaDu cells is hypothesized to reduce STAT3 phosphorylation and subsequently decrease the expression of these target genes encoding anti-apoptotic proteins, thereby initiating apoptosis through the mitochondrial pathway (Figure 8)."
sparser
"EGFR V948R transfection retained STAT3 phosphorylation inEGFR −/− ,TMEM25 −/− TNBC cells, strongly suggesting that EGFR can phosphorylate STAT3 in the monomeric form in the absence of TMEM25 and thereby relays sustainable proliferative signals to cancer cells to provide the growth advantage."
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"In contrast, pStat3 level, which was higher in Gprc5a -/- cells than in Gprc5a +/+ cells before EGF treatment, decreased 30 min after EGF addition and began to increase slightly after 3 hours (XREF_FIG, middle) suggesting that EGFR activation does not mediate Stat3 phosphorylation in either of these cells."
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"The C-E-Cad 14-aa tail enables direct binding to the CR2 domain of full-length EGFR through salt bridge and hydrogen bond interactions, accompanied by EGFRvIII to promote STAT3 phosphorylation and nuclear translocation and AKT and ERK1/2 phosphorylation, resulting in the tumorigenicity of GBM [46, 105]."
| PMC
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"The C-E-Cad 14-aa tail enables direct binding to the CR2 domain of full-length EGFR through salt bridge and hydrogen bond interactions, accompanied by EGFRvIII to promote STAT3 phosphorylation and nuclear translocation and AKT and ERK1/2 phosphorylation, resulting in the tumorigenicity of GBM [46, 105]."
| PMC
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"Although the safety and efficacy of dupilumab have been interpreted in atopic dermatitis and asthma,46, 47, 48 the dose and impact on osimertinib resistance in NSCLC patients need to be confirmed by clinical studies.In conclusion, we demonstrate that EGFR T790M-cis-L792F mutation in lung adenocarcinoma upregulated Jak and STAT3 phosphorylation and increased IL-4 production via specifically binding to IL4 promoter, which promotes M2 macrophages polarization and induces resistance to osimertinib."
sparser
"Together
with our previous finding that VGF-induced EGFR activates non-canonical STAT3
phosphorylation to increase TCA cycle intermediate levels ( xref ), these findings highlight VGF’s multiple roles in
rewiring host metabolism during VACV infection by modulating various cellular
signaling pathways and metabolic processes."
reach
"Interestingly, although the increase amount of STAT3 phosphorylation induced by EGFR is similar under different serum conditions, it is noteworthy that its percentage to the total STAT3 phosphorylation was dramatically higher in low serum conditions, suggesting that this EGFR-mediated STAT3 phosphorylation may has a more potent role for cells in low serum conditions."
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"Furthermore, we reconstituted the phosphorylation reaction of STAT3 in vitro using bacterially produced STAT3 and Flag-tagged EGFR affinity purified from HEK293T cells (Fig. 4i), which is in good agreement with previous report that STAT3 can be directly phosphorylated by EGFR in vitro ."
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"In line with the binding assays (Fig. 4f–h), presence of TMEM25-C attenuated EGFR-mediated phosphorylation of STAT3 in a dose-dependent manner (Fig. 4i), suggesting that TMEM25 prevents EGFR-mediated phosphorylation of STAT3 by competitively binding to the cytosolic domain of EGFR."
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"However, in contrast to EGFR-D837N that could not rescue the STAT3 phosphorylation, EGFR-V948R showed a remarkable effect on rescuing the STAT3 phosphorylation as wild-type EGFR did, although its efficacy was to some extent lower than that of wild-type EGFR (Fig. 5b and Supplementary Fig. 8a), suggesting that, in the absence of TMEM25, the phosphorylation of STAT3 by EGFR only requires the kinase activity of EGFR but not necessarily dimer formation or phosphorylation of Y1068 and Y1086."