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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: Anticancer Agents Med Chem. 2013 May 1;13(4):576–580. doi: 10.2174/1871520611313040006

Fig. 3. The cross-linked signaling between FAK, p53, Mdm-2, and Nanog in cancer stem cells.

Fig. 3

P53 binds FAK promoter and inhibits its promoter activity. FAK sequesters p53 from apoptotic signaling and blocks p53-transcriptional activity. FAK binds Mdm-2 to facilitate p53 ubiquitination and degradation. P53 up-regulates Mdm-2, and represses Nanog. Furthermore, Nanog represses p53 to maintain cancer stem cell pool and block differentiation, cell cycle arrest, apoptosis and other cell growth inhibiting p53 functions to promote tumor growth. Nanog up-regulates FAK, and FAK is able to phosphorylate Nanog and this cross-linked signaling mediates cell motility and invasion of cancer stem cells and play s significant role in tumor metastasis.