FAK and Nanog Cross Talk with p53 in Cancer Stem Cells

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


Volume 14, 10 Issues, 2014


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Anti-Cancer Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Cancer Agents

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  • 85th of 202 in Oncology

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Editor-in-Chief:
Michelle Prudhomme
Universite Blaise Pascal - C.N.R.S
Aubiere Cedex
France


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FAK and Nanog Cross Talk with p53 in Cancer Stem Cells

Author(s): Vita M. Golubovskaya

Affiliation: Department of Surgical Oncology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY, 14263, USA.

Abstract

This review is focused on the role of Focal Adhesion Kinase (FAK) signaling in cancer stem cells. The recent data demonstrate the important role of FAK in cancer stem cell proliferation, differentiation, motility, and invasion. We showed recently that the transcription factor Nanog binds the FAK promoter and up-regulates FAK expression, and that FAK binds Nanog and phosphorylates it. This review discusses the interaction of FAK, Nanog, Oct-3/4, and Sox-2 signaling pathways that are critical for the regulation of cancer stem cells. The cross-linked signaling of FAK with p53 and Nanog signaling in cancer stem cell and function and targeted therapeutics approaches are discussed.

Keywords: Adhesion, Cancer, Focal Adhesion Kinase, Inhibitor, Metastasis, Tumor

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Article Details

Volume: 13
Issue Number: 4
First Page: 576
Last Page: 580
Page Count: 5
DOI: 10.2174/1871520611313040006
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