Focal Adhesion Kinase and p53 signal transduction pathways in cancer

被引：62

作者：

Golubovskaya, Vita M. ^{[1
]}

Cance, William ^{[1
]}

机构：

[1] Roswell Pk Canc Inst, Dept Surg Oncol, Buffalo, NY 14263 USA

来源：

FRONTIERS IN BIOSCIENCE-LANDMARK | 2010年 / 15卷

关键词：

Focal Adhesion Kinase; p53; cancer; Protein Interaction; Inhibitors; Tumorigenesis; Small Molecules; MDM-2; Survival; Apoptosis; Review; AMINO-TERMINAL DOMAIN; PROTEIN-TYROSINE KINASE; HUMAN BREAST; CELL-SURVIVAL; NEGATIVE REGULATION; STRUCTURAL BASIS; FAK EXPRESSION; DEATH-DOMAIN; KAPPA-B; OVEREXPRESSION;

D O I：

10.2741/3653

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

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.

引用

页码：901 / 912

页数：12

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