Paradoxical roles of FAK in tumor cell migration and metastasis.
Focal adhesion kinase (FAK), as a key mediator of signaling induced by integrins, plays an instrumental role in many cellular functions, including cell survival and proliferation. Many studies have reported that FAK is a positive regulator of normal cell migration and cancer cell metastasis. However, emerging evidence shows that FAK--under certain oncogenic signaling, such as that initiated by activated Ras and some growth factor receptor kinases--negatively regulates cancer cell migration. Activated Ras may promote tumor cell migration by dephosphorylation of FAK at Y397 and facilitation of focal adhesion turnover at the leading edge of cells.
Zheng
Yanhua
Y
Brain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Lu
Zhimin
Z
D000818:Animals; D002448:Cell Adhesion; D002465:Cell Movement; D051416:Focal Adhesion Protein-Tyrosine Kinases / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000502:physiology; D011905:Genes, ras / Q000502:physiology; D006801:Humans; D016023:Integrins / Q000378:metabolism; D051379:Mice; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000201:enzymology / Q000473:pathology*; D051419:Paxillin / Q000378:metabolism*; D010766:Phosphorylation / Q000502:physiology; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology
D016023:Integrins; D051419:Paxillin; D020794:Receptor Protein-Tyrosine Kinases; D051416:Focal Adhesion Protein-Tyrosine Kinases