CELL-ADHESION AND REGULATORY MOLECULES INVOLVED IN TUMOR-FORMATION, HEMOSTASIS, AND WOUND-HEALING

Background. Dynamic changes in cell adhesion and migration are fundamental properties of the cells that are important in hemostasis, vascularization, and wound repair. Changes in cell adhesion and migration are very important in the formation of tumors, and invasion and metastasis by neoplasms. Methods. Using immunolocalization and immunopurification techniques, expression of integrin molecules involved in cell adhesion has been characterized during tumor development and wound healing. The ability of cytokines to regulate expression and antibody and peptide inhibitors to inhibit function of integrins has been explored to better understand the role of integrins in pathogenesis. Results. Increased suprabasilar expression or the integrins alpha 6 beta 4, alpha 2 beta 1, and alpha 3 beta 1 accompanies development of squamous cell neoplasms of the head and neck. Integrin alpha II beta 3 is an integrin receptor which is important in platelet aggregation in hemostasis and formation of tumor metastases. Increased expression of integrin alpha v beta 3 has been identified in angiogenesis in response to growth factors and tumor angiogenic factors. Cytokine TGF-beta and arachadonic acid metabolite 12(S)-HETE are important signals in regulation of integrins and affect cell aggregation and migration in these processes. Ligands and inhibitors for some of these receptors have been identified which will be useful in determining their role during tumor development and progression. Conclusions. Recent advances in understanding the functions of the integrin cell adhesion molecules may soon add new diagnostic methods and therapies to the armamentarium of the head and neck oncologic, microvascular, plastic, and reconstructive surgeon. Therapies directed at controlling integrin cell-adhesion molecule expression and function are being explored to improve scar formation, bone synthesis, inhibition of vascular occlusion, and inhibition of tumor invasion and metastasis. (C) 1995 John Wiley and Sons, Inc.