Focal adhesion kinase (FAK) plays a vital role in tumor cell proliferation, survival and migration. Altered metabolic pathways fuel rapid tumor growth by accelerating glucose, lipid and glutamine processing. Besides the mitogenic effects of FAK, evidence is accumulating supporting the association between hyper-activated FAK and aberrant metabolism in tumorigenesis. FAK can promote glucose consumption, lipogenesis, and glutamine dependency to promote cancer cell proliferation, motility, and survival. Clinical studies demonstrate that FAK-related alterations of tumor metabolism are associated with increased risk of developing solid tumors. Since FAK contributes to the malignant phenotype, small molecule inhibition of FAK-stimulated bioenergetic and biosynthetic processes can provide a novel approach for therapeutic intervention in tumor growth and invasion.
Keywords: Focal adhesion kinase; Glutamine; Lipogenesis; Molecular targeting; Motility; Proliferation.
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