IndraLab

Statements


SRC increases the amount of EGFR. 8 / 13
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"FHL1 interacts with the transcription factor SP1 to upregulate EGFR expression and activate the downstream signaling cascades, including Src, Akt, Erk1/2, and Stat3, leading to glioblastoma malignancy."

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"Parsons et al. first showed c-Src overexpression in EGFR expressing metastatic breast and other cancer cells promoted cell migration XREF_BIBR."

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"Knockdown of c-Src inhibited UVB-induced COX-2 expression and phosphorylation of MAPKs and EGFR in HaCaT cells."

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"Consistent with these findings, siRNA silencing of Src also effectively reduced in vitro invasion of EGFR expressing LN229 glioblastoma cells (XREF_FIG)."

"ET-1, as well as PGE2, induced HEY and OVCA433 cells revealed a significant increase in the level of phosphorylated EGFR. Pretreatment of HEY cells with the specific EGFR kinase inhibitor, AG1478, as well as with the Src tyrosine kinase inhibitor, PP2 significantly reduced both ET-1 and PGE2 induced EGFR phosphorylation, indicating that activation of Src is essential for ET-1- and PGE2 induced EGFR transactivation. The interruption of EGFR signaling induced by AG1478, as well as by PP2, resulted in a concomitant reduction of PGE2 secretion, as well as of VEGF expression at protein and mRNA levels, indicating that Src mediated EGFR transactivation is involved in ET-1 induced PGE2 and VEGF production."

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"The constitutively activated Src allele did not initially enhance growth of EGFRvIII expressing tumors, but eventually conferred a modest growth enhancement once the tumors had become very large (XREF_FIG, p = 0.03)."

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"Indeed, this treatment increases EGFR expression, induces Src activation and caveolae mediated EGFR endocytosis."

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"Our results showed that overexpression of EGFR or activated Src partially reduced YC-1-mediated growth inhibition, indicating their potential involvement in the anti-proliferative mechanism of YC-1."