IndraLab
Statements
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"Importantly, TRPM7 mediated calcium signals further modulate EMT in breast cancer cells, which TRPM7 deficiency specifically reduces EGF-induced STAT3 phosphorylation and the expression of Vimentin, suggesting that TRPM7 is required for maintaining a mesenchymal feature in breast cancer cells ( xref )."
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"Similar as MAPK and AKT activation, basal STAT3 activity is not changed by depleting any isoforms of PIPKIgamma comparing to control cells, whereas STAT3 phosphorylation stimulated by EGF was inhibited in pan-PIPKIgamma depleted L3.6 cells, suggesting the requirement of PIPKIgamma in growth factor induced activation of JAK2 and STAT3 pathway."
sparser
"Similar as MAPK and AKT activation, basal STAT3 activity is not changed by depleting any isoforms of PIPKIγ comparing to control cells, whereas STAT3 phosphorylation stimulated by EGF was inhibited in pan-PIPKIγ depleted L3.6 cells (Figure xref ), suggesting the requirement of PIPKIγ in growth factor-induced activation of JAK2/STAT3 pathway."
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"We have recently found that PYK2 is a common downstream effector of EGFR and c-Met; and have delineated their crosstalk signalling in TNBC, demonstrating that knockdown of PYK2 facilitates receptor degradation and concomitantly inhibits EGF-induced ERK1/2 and STAT3 phosphorylation."
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"EGF significantly induced STAT3 phosphorylation and elevated the mRNA levels of LGR5 in the HT29 cells (Fig. xref ), implying that addition of EGF activated STAT3 in the cancer stem-like tumorspheres, thus contributing to the formation and survival of EGFR-positive CRC stem-like tumorspheres."
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"Treatment of immune cells (particularly T cells) with interleukin-6 (IL-6), IL-10, hepatocyte growth factor, epidermal growth factor, as well as other growth factors and cytokines, promotes Stat3 phosphorylation, and consequently Stat3 translocation to the nucleus, where it binds specific DNA sequences and promotes gene expression [XREF_BIBR]."
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"We evaluated whether desensitization of EGF-induced STAT3 phosphorylation could be associated with GRB2 up-regulation and/or increased association of Grb2 to the EGFR in the transgenic mice overexpressing GH, but no significant differences in GRB2 protein content or GRB2 association to EGFR between normal and transgenic mice were found ( xref )."
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"Exposure to sorafenib transiently reduced EGF-dependent STAT3 phosphorylation in MM1 (maximum –37% after 30 min) and MM4 (maximum –40% after 30 min) cells, whereas in MM3 cells a sustained dephosphorylation starting 30 min after treatment (–55%) and lasting for the entire experimental period was observed (Fig. xref )."
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"In accordance with a previous study [ xref ], we observed an increase in STAT3 phosphorylation by EGF; of note, tyrosine-705 phosphorylation was transient, while serine-727 phosphorylation was long-lasting over 60 min (Figure xref ), suggesting that serine phosphorylation of STAT3 may play a role in CCR1 expression."
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"The gefitinib sensitive SRC (v-src sarcoma viral oncogene homolog) phosphorylation site Tyr845 on EGFR has been shown to mediate activation of STAT3, and indeed loss of EGF dependent phosphorylation of STAT3 in response to gefitinib appears to be tightly coupled to suppression of EGFR autophosphorylation (Sato et al, 2003; Shao et al, 2003)."
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"EGF significantly induced STAT3 phosphorylation and elevated the mRNA levels of LGR5 in the HT29 cells (Fig. 4d), implying that addition of EGF activated STAT3 in the cancer stem-like tumorspheres, thus contributing to the formation and survival of EGFR-positive CRC stem-like tumorspheres."
sparser
"In particular, interleukin-6 (IL-6) or epidermal growth factor (EGF) stimulate the phosphorylation of STAT3 protein by Janus kinase and activated STAT3 forms a homodimer that translocates to the nucleus where it regulates the expression of genes critical for normal cellular processes such as cell development, differentiation, proliferation, survival, angiogenesis, and immune function xref – xref ."
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"More specifically, IL-8, IL-6, and EGF induce phosphorylation of STAT3 and ERK in the endothelial cells resulting in their increased survival and proliferation to promote angiogenesis. xref CAF-secreted CXCL12 via CXCL12/CXCR4 signaling in endothelial cells controls angiogenesis by upregulating VEGF expression. xref TGF-β, which is present in the HNSCC TME and also secreted by Tregs, CAFs, TAMs, and MSDCs also increase angiogenesis. xref Similarly, lymphotoxin-α (LT-α), a member of the TNF superfamily, and an important pro-inflammatory cytokine secreted by B and T lymphocytes, increases angiogenesis by regulating CXCL2 expression."
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"To identify the signal pathway or the protein kinase that regulates the interaction between Cdc25A and PKM2, we pretreated U87/EGFR cells with the following inhibitors: the phosphoinositide 3-kinase inhibitor LY294002, c-Jun N-terminal kinases (JNK) inhibitor SP600125, a NF-κB inhibitor, a JAK2 inhibitor and Src inhibitor SU6656, which blocked EGF-induced phosphorylation of AKT and c-Jun, TNF-α-induced and NF-κB-dependent IκBα promoter activation, and EGF-induced phosphorylation of Stat3 and c-Src, respectively ( xref )."
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"In A431 cells, a human epidermoid carcinoma cell line, that endogenously expresses high levels of epidermal growth factor receptor, it was shown that c-Src kinase activity was required for the epidermal growth factor-induced tyrosine phosphorylation of STAT1, STAT3, and STAT5 ( xref )."
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"Our results reveal that EGF (10 ng/mL) did not induce STAT3 phosphorylation in pRCC cells compared to vehicle control at either 10 min or 12 h timepoints (Fig. 7B), and moreover, AG1478 (500 nM) did not affect STAT3 phosphorylation either alone or in the presence of EGF, suggesting that in ACHN pRCC cells, EGFR is not an upstream regulator of STAT3 (Fig. 7B)."
sparser
"The gefitinib-sensitive SRC (v-src sarcoma viral oncogene homolog) phosphorylation site Tyr845 on EGFR has been shown to mediate activation of STAT3, and indeed loss of EGF-dependent phosphorylation of STAT3 in response to gefitinib appears to be tightly coupled to suppression of EGFR autophosphorylation ( xref ; xref )."
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"Thus, while TRPM7 regulates some elements of EGF induced EMT (i.e. vimentin protein induction and STAT3 phosphorylation), EGF induced increases in the mRNA levels of other EMT markers (i.e. Twist and N-cadherin) (XREF_SUPPLEMENTARY), and EGF induced changes in cell morphology (XREF_SUPPLEMENTARY), are not affected by modulation of TRPM7, suggesting that other transporters of calcium are likely to be involved in the other aspects of calcium dependent EMT induction demonstrated by calcium chelation."