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. Author manuscript; available in PMC: 2010 Apr 1.
Published in final edited form as: Cell Signal. 2008 Dec 7;21(4):470–476. doi: 10.1016/j.cellsig.2008.11.015

Fig. 1.

Fig. 1

Mechanisms of carcinoma cell migration mediated by Akt. Breat carcinoma cells respond to IGF-1 leading to activation of PI 3-K and in turn phosphorylation and activation of Akt1 and Akt2. Akt1 can function to suppress carcinoma cell migration by various redundant mechanisms, inducing degradation of NFAT and attenuation of pro-invasion and metastasis genes. Akt1 can also suppress ERK and TSC2 activity leading to suppression of migration. In contrast, Akt2 functions to enhance carcinoma cell migration, in part by up-regulating β1 integrins and other yet to be determined mechanisms.