title: Reciprocal control of cell proliferation and migration.
abstract: In adult tissue the quiescent state of a single cell is maintained by the steady state conditions of its own microenvironment for what concern both cell-cell as well as cell-ECM interaction and soluble factors concentration. Physiological or pathological conditions can alter this quiescent state through an imbalance of both soluble and insoluble factors that can trigger a cellular phenotypic response. The kind of cellular response depends by many factors but one of the most important is the concentration of soluble cytokines sensed by the target cell. In addition, due to the intrinsic plasticity of many cellular types, every single cell is able, in response to the same stimulus, to rapidly switch phenotype supporting minimal changes of microenviromental cytokines concentration. Wound healing is a typical condition in which epithelial, endothelial as well as mesenchymal cells are firstly subjected to activation of their motility in order to repopulate the damaged region and then they show a strong proliferative response in order to successfully complete the wound repair process. This schema constitute the leitmotif of many other physiological or pathological conditions such as development vasculogenesis/angiogenesis as well as cancer outgrowth and metastasis.Our review focuses on the molecular mechanisms that control the starting and, eventually, the switching of cellular phenotypic outcome in response to changes in the symmetry of the extracellular environment.
authors.affiliation: Dipartimento di Scienze Biochimiche, Università di Firenze, Viale Morgagni 50, 50134 Firenze, Italy. paolo.cirri@unifi.it.
authors.forename: Alina
authors.initials: A
authors.lastname: De Donatis
authors.forename: Francesco
authors.initials: F
authors.lastname: Ranaldi
authors.forename: Paolo
authors.initials: P
authors.lastname: Cirri
references.citation: Mol Cell Biol. 1994 Mar;14(3):1680-8
references.pmid: 7509446
references.citation: Cytokine Growth Factor Rev. 2004 Aug;15(4):205-13
references.pmid: 15207812
references.citation: Mol Cell. 2010 Feb 12;37(3):321-32
references.pmid: 20159552
references.citation: Cancer Res. 2009 Feb 15;69(4):1383-91
references.pmid: 19208836
references.citation: J Biol Chem. 2008 Jul 18;283(29):19948-56
references.pmid: 18499659
references.citation: J Biol Chem. 2003 Aug 22;278(34):32027-36
references.pmid: 12783862
references.citation: Proc Natl Acad Sci U S A. 2005 Feb 22;102(8):2760-5
references.pmid: 15701692
references.citation: Cell. 2000 Oct 13;103(2):211-25
references.pmid: 11057895
references.citation: Physiol Rev. 1999 Oct;79(4):1283-316
references.pmid: 10508235
references.citation: Dev Cell. 2005 Aug;9(2):197-207
references.pmid: 16054027
references.citation: Curr Opin Cell Biol. 2004 Aug;16(4):400-6
references.pmid: 15261672
references.citation: Mol Cell Biol. 2004 Sep;24(18):8113-33
references.pmid: 15340073
references.citation: Trends Cell Biol. 2001 Dec;11(12):504-11
references.pmid: 11719057
references.citation: Trends Cell Biol. 2006 May;16(5):257-63
references.pmid: 16581250
references.citation: Nat Rev Mol Cell Biol. 2001 Apr;2(4):294-307
references.pmid: 11283727
references.citation: Cell. 2006 Mar 10;124(5):897-900
references.pmid: 16530038
references.citation: J Biol Chem. 2004 Feb 27;279(9):8038-46
references.pmid: 14660565
references.citation: Commun Integr Biol. 2008;1(2):156-7
references.pmid: 19704878
references.citation: Mol Cell Biol. 1995 Feb;15(2):954-63
references.pmid: 7529876