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. 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 4. FAK modulation of cancer cell metabolism.

Fig 4.

Insulin/IGF1 stimulates FAK-PI3K-Akt signaling through IRS. This modulates glucose metabolism via activation of glucose transporters, glycolytic and mitochondrial enzymes. Citrate can leave the TCA cycle in mitochondria and is converted to lipids. FAK activation of ERK/Akt can promote this conversion and channel glucose to lipids for the biosynthetic needs of rapidly growing cells. Anchorage-dependent stimulation of FAK activity contributes to K-Ras/Myc signaling-related glutamine metabolism.

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