Cell adhesion proteins as tumor suppressors.
OBJECTIVE
We summarize recent progress on the role of cell adhesion molecules in biology and discuss the potential application of cell adhesion molecules for managing urological cancer.


METHODS
We comprehensively reviewed the literature from 1982 to 2001, including peer reviewed publications and recent abstracts from national meetings, relevant to cell adhesion molecules in urological cancer.


RESULTS
A growing body of evidence suggests that alterations in the adhesion properties of neoplastic cells have a pivotal role in the development and progression of cancer. Loss of intercellular adhesion and desquamation of cells from the underlying lamina propria allows malignant cells to escape from their site of origin, degrade the extracellular matrix, acquire a more motile and invasion phenotype, and invade and metastasize. In addition to participating in tumor invasiveness and metastasis, adhesion molecules regulate or significantly contribute to various functions, including signal transduction, cell growth, differentiation, site specific gene expression, morphogenesis, immunological function, cell motility, wound healing and inflammation. To date a diverse system of transmembrane glycoproteins has been identified that mediates cell-cell and cell-extracellular matrix adhesion. The main families of adhesion molecules include members of the Ig superfamily, cadherins, integrins and selectins.


CONCLUSIONS
Multiple and diverse cell adhesion molecules participate in intercellular and cell-extracellular matrix interactions of cancer. Cancer progression is a multistep process, in which some adhesion molecules have a pivotal role in the development of recurrent, invasive and distant metastasis. Recent data implicate some of these molecules in cell signaling and tumor suppression, which has important consequences for tumor growth.
Okegawa
Takatsugu
T
Department of Urology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9110, USA.
Li
Yingming
Y
Pong
Rey-Chen
RC
Hsieh
Jer-Tsong
JT
D000251:Adenosine Triphosphatases / Q000187:drug effects / Q000502:physiology; D015703:Antigens, CD; D015820:Cadherins / Q000187:drug effects / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D016023:Integrins / Q000187:drug effects / Q000502:physiology; D018799:Intercellular Adhesion Molecule-1 / Q000187:drug effects / Q000502:physiology; D011991:Receptors, Virus / Q000187:drug effects / Q000502:physiology; D014571:Urologic Neoplasms / Q000188:drug therapy*
D015703:Antigens, CD; C069847:CD66 antigens; D015820:Cadherins; D015815:Cell Adhesion Molecules; D016023:Integrins; D011991:Receptors, Virus; C085301:adenovirus receptor; C105941:coxsackievirus B receptor; D018799:Intercellular Adhesion Molecule-1; D000251:Adenosine Triphosphatases