Library Subscription: Guest
Begell Digital Portal Begell Digital Library eBooks Journals References & Proceedings Research Collections
Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2.2

ISSN Print: 0893-9675
ISSN Online: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v8.i4.40
pages 343-358

Role of Focal Adhesion Proteins in Signal Transduction and Oncogenesis

Ellen Weisberg
Division of Cell Biology, Harvard Medical School, Boston MA 02115
Martin Sattler
Dana-Farber Cancer Institute, Department of Adult Oncology and Division of Medicine, Brigham and Women's Hospital
Darren S. Ewaniuk
Department of Adult Oncology, Dana-Farber Cancer Institute
Ravi Salgia
Department of Medical Oncology and Therapeutics Research, Comprehensive Cancer Center, City of Hope National Medical Center


The focal adhesion is a structure that is formed when a cell comes into contact with the extracellular matrix. Originally, the focal adhesion was thought to only provide structural support for the actin-based cytoskeleton of the cell. However, the last decade has yielded considerable information linking various protein components of the focal adhesion to signal transduction pathways. Examples of focal adhesion proteins include the catalytically active pl25FAK, SH2-containing tensin, and the multifunctional LIM domain-containing paxillin. The interactions of focal adhesion proteins may be altered after cellular transformation. This review details how certain focal adhesion proteins are associated in cellular signaling as well as transformation. The importance of various GTP-binding proteins in interacting with and forming the focal adhesion, and the influence they have on neoplastic transformation, are discussed. A key feature of this review is how oncogenes and their respective oncoproteins affect the focal adhesion. Classically, ν-src transformation of adherent cells has been studied to characterize focal adhesions, namely, because of the distinct morphological changes that occur in the focal adhesion concomitantly with src transformation. Similarly, the BCR/ABL oncogene, which causes chronic myelogenous leukemia, leads to adhesion defects and can alter the properties of focal adhesion proteins. Thus, we describe some of the relevant interactions between the focal adhesion and the Src and BCR/ABL oncoproteins, respectively.

Articles with similar content:

Regulation of FAK Activity by Tetraspan Proteins: Potential Clinical Implications in Cancer
Critical Reviews™ in Oncogenesis, Vol.20, 2015, issue 5-6
Yu Qin, Lynn Gordon, Madhuri Wadehra, Shabnam Mohandessi
Signal Transduction and Actin in the Regulation of G1-Phase Progression
Critical Reviews™ in Eukaryotic Gene Expression, Vol.15, 2005, issue 3
Maarten J. A. Moes, Johannes Boonstra
Role of the Cytoskeletal Protein Paxillin in Oncogenesis
Critical Reviews™ in Oncogenesis, Vol.11, 2000, issue 1
Paul T. Morrison, Ravi Salgia, Martin Sattler, Evan Pisick
Protein Kinase C Control of Gene Expression
Critical Reviews™ in Eukaryotic Gene Expression, Vol.11, 2001, issue 1-3
Carlo Ventura, Margherita Maioli
T Lymphocyte Migration: The Influence of Interactions via Adhesion Molecules, the T Cell Receptor, and Cytokines
Critical Reviews™ in Immunology, Vol.15, 1995, issue 3-4
Julius Klominek, Sten-Erik Bergstrom, Dan Hauzenberger, Karl-Gosta Sundqvist