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. 2018 Jul 11;9:907. doi: 10.3389/fphys.2018.00907

FIGURE 1.

FIGURE 1

Schematic overview of the GPR30/EGFR/PI3K/STAT signaling axis. This network consists of the interaction between GPR30/PI3K/MAPK/STAT pathways. Initial stimulation by tamoxifen causes activation of GPR30 receptors and activation of PLC by releasing the Gβγ subunit which can trigger ERK activation. Also, src can activate MMPs which can convert HB-EGF to EGF. EGF can bind and activate EGFR, causing receptor dimerization and cross-phosphorylation of tyrosine residues in the intracellular domains. The activated EGFR axis can phosphorylate ERK and through that regulates various cell processes. PI3K and JAK can be recruited to cell membrane by interaction with EGFR phosphotyrosine docking sites. PI3K subsequently causes AKT activation and regulates cell growth and survival. Activation of STAT dimers by JAK play a key role in controlling cell growth and survival. Since JAK-STAT signaling can allow the transcription of genes involved in cell division, one potential effect of excessive JAK-STAT signaling is cancer formation.