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. 2020 Nov 10;21(22):8422. doi: 10.3390/ijms21228422

Figure 2.

Figure 2

Schematic representation of FAK involvement in tumor growth and metastasis. (a) FAK is autophosphorylated in response to growth factor receptors and integrins activation and activated by Src. (b) Active FAK promotes tumor cell invasion and metastasis, activating PI3K-AKT-mTOR signaling cascade, which results in increased NFkB transcriptional activity. (c) Active FAK also stimulates cytoskeletal remodeling and focal adhesion formation/turnover, inducing SRC-dependent phosphorylation of paxillin and p130cas, leading to the formation of a focal adhesion complex which includes phosphorylated/active FAK, paxillin, and p130cas. SRC also stimulates ERK signaling cascade which results in the ETS transcription factor-dependent induction of cyclin D1 (CycD1) expression which in turn promotes tumor cell survival and growth. (d) Nuclear FAK acts as a scaffold protein for the p53–MDM2 interaction, inducing p53 ubiquitination and its proteasomal degradation which results in apoptosis inhibition. Figure realized with BioRender.com.