Skip to main content
. Author manuscript; available in PMC: 2019 Jan 28.
Published in final edited form as: Pharmacol Ther. 2013 Dec 9;142(2):154–163. doi: 10.1016/j.pharmthera.2013.12.003

Fig 1. FAK modulation of cancer cell glucose consumption and proliferation.

Fig 1.

Growth factors, insulin/IGF1R, and/or anchorage-activated integrin trigger FAK activation. Downstream factors, IRS and PI3K/Akt induce alteration of glycolysis and mitochondrial respiration. Excessive glucose consumption provides energy and precursors to rapidly growing cells. Inhibitors targeting FAK or FAK-IGF1R interactions can prevent malignant cell glucose consumption and growth.

HHS Vulnerability Disclosure