Protein Kinase B/AKT and Focal Adhesion Kinase: Two Close Signaling Partners in Cancer

ISSN: 1875-5992 (Online)
ISSN: 1871-5206 (Print)

Volume 17, 14 Issues, 2017

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Anti-Cancer Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Cancer Agents

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Michelle Prudhomme
Institut de Chimie de Clermont-Ferrand
Université Clermont Auvergne

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Protein Kinase B/AKT and Focal Adhesion Kinase: Two Close Signaling Partners in Cancer

Anti-Cancer Agents in Medicinal Chemistry, 11(10): 993-1002.

Author(s): Shouye Wang and Marc D Basson.

Affiliation: Department of Surgery, Michigan State University, 1200 East Michigan Avenue, Suite No. 655, Lansing, MI 48912, USA.


AKT (or protein kinase B) and focal adhesion kinase (FAK) are two important kinases that regulate various cellular functions. Each is overexpressed and/or aberrantly activated in diverse cancers. Several small molecular inhibitors targeting either AKT or FAK are in development or in clinical trials. It is well established that FAK is an upstream regulator of AKT signaling pathway in various cancer cell lines and in xenograft tumor models. However, very recent reports from our laboratory and others demonstrate that AKT can also directly regulate FAK through direct association and serine phosphorylation. This indicates that AKT and FAK may be dual therapeutic targets for pharmacologic intervention in the treatment of primary and metastatic cancer. FAK-AKT interaction is particularly critical for metastatic adhesion. We review recent developments in AKT and FAK signaling in cancer with the particular emphasis on the novel signaling pathways in which FAK is downstream of AKT. We also provide an update on inhibitors targeting AKT or FAK currently in clinical trials.


AKT, AKT1, AKT2, cancer, cancer metastasis, cell signaling, differentiation, FAK, FERM, invasion, isoform, migration, proliferation, Src.

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Article Details

Volume: 11
Issue Number: 10
First Page: 993
Last Page: 1002
Page Count: 10
DOI: 10.2174/187152011797927661
Price: $58

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