title: Contact inhibition (of proliferation) redux.
abstract: It has long been appreciated that proliferation of many cells is inhibited by density, a phenomenon that is often attributed to cell-cell contact. The basic properties of this phenomenon were established in the 1960s, along with the observation that such density-dependence was also lost in transformed cells. The mechanistic basis of contact inhibition of proliferation (CIP) has been slower to reveal itself. Here we discuss recent progress in elucidating the roles that cell-cell adhesion molecules play as receptors for CIP and in characterising the intracellular signaling pathways that mediate adhesion-dependent proliferative inhibition.
authors: Massachusetts General Hospital Center for Cancer Research and Harvard Medical School Department of Pathology, Charlestown, MA, USA. mcclatch@helix.mgh.harvard.edu
authors: Andrea I
authors: AI
authors: McClatchey
authors: Alpha S
authors: AS
authors: Yap
mesh_terms: D000818:Animals; D015820:Cadherins / Q000378:metabolism; D051177:Catenins / Q000378:metabolism; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000378:metabolism; D049109:Cell Proliferation; D003260:Contact Inhibition / Q000502:physiology*; D003599:Cytoskeleton / Q000378:metabolism; D006801:Humans; D040542:Mechanotransduction, Cellular; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D017978:Receptors, Growth Factor / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D015820:Cadherins; D051177:Catenins; D015815:Cell Adhesion Molecules; D017978:Receptors, Growth Factor; D017346:Protein Serine-Threonine Kinases