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Focal adhesion kinase and p53 signal transduction pathways in cancer
Vita M Golubovskaya1,William Cance1
1
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. Vita.Golubovskaya@Roswellpark.org
DOI: 10.2741/3653 Volume 15 Issue 3, pp.901-912
Published: 01 June 2010
(This article belongs to the Special Issue Focal adhesion signaling in cancer)
Abstract

Human cancer is characterized by a process of tumor cell motility, invasion, and metastasis. One of the critical tyrosine kinases that is linked to these processes of tumor invasion and survival is the Focal Adhesion Kinase (FAK). Our laboratory was the first to isolate FAK from human tumors, and we had demonstrated that FAK mRNA was up-regulated in invasive and metastatic human breast and colon cancer samples. We have cloned FAK promoter and have found that FAK promoter contains p53 binding sites, and that p53 inhibits FAK transcription and regulates its expression in tumor samples. In addition, we have found a high correlation between FAK overexpression and p53 mutations in 600 population-based series of breast cancer patients. found that N-myc binds FAK promoter and induces FAK transcription in neuroblastoma cells. Thus, this review will be focused on FAK and p53 signal transduction pathways in cancer.

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Vita M Golubovskaya, William Cance. Focal adhesion kinase and p53 signal transduction pathways in cancer. Frontiers in Bioscience-Landmark. 2010. 15(3); 901-912.