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. Author manuscript; available in PMC: 2019 Sep 16.
Published in final edited form as: Curr Pharm Des. 2017 Nov 16;23(29):4226–4246. doi: 10.2174/1381612823666170616082125

Figure 3. EGF/EGFR signal transduction and its targeted therapy.

Figure 3.

The binding of EGF to its receptor initiates a variety of signaling cascade via five main pathways; 1) RAS/RAF/MAPK, 2) PI3K/AKT, 3) JAK/STAT, 4) PLCγ/PKC/Ca2+-dependent, and 5) Src/FAK/MMP. Furthermore, the EGF/EGFR dimer can directly regulate the expression of specific genes through an endocytosis mechanism. Constitutive activation of EGFR as a result of mutation of the EGFR gene can promote cancer by facilitating DNA synthesis, cell proliferation, angiogenesis, invasion, and metastasis. Ongoing clinical trials of anticancer drugs, like monoclonal antibodies of the EFG binding site or small molecules against the EGF catalytic domain, may prove to inhibit EGF/EGFR signaling by blocking its autophosphorylation.