Outside-in signaling through integrins and cadherins:: A central mechanism to control epidermal growth and differentiation?

被引:125
作者
Mueller, Eliane J. [1 ]
Williamson, Lina [1 ]
Kolly, Carine [1 ]
Suter, Maja M. [1 ]
机构
[1] Univ Bern, Inst Anim Pathol & DermFocus, Vetsuisse Fac, CH-3001 Bern, Switzerland
关键词
D O I
10.1038/sj.jid.5701248
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
The process of epidermal renewal persists throughout the entire life of an organism. It begins when a keratinocyte progenitor leaves the stem cell compartment, undergoes a limited number of mitotic divisions, exits the cell cycle, and commits to terminal differentiation. At the end of this phase, the postmitotic keratinocytes detach from the basement membrane to build up the overlaying stratified epithelium. Although highly coordinated, this sequence of events is endowed with a remarkable versatility, which enables the quiescent keratinocyte to reintegrate into the cell cycle and become migratory when necessary, for example after wounding. It is this versatility that represents the Achilles heel of epithelial cells allowing for the development of severe pathologies. Over the past decade, compelling evidence has been provided that epithelial cancer cells achieve uncontrolled proliferation following hijacking of a "survival program" with PI3K/Akt and a "proliferation program" with growth factor receptor signaling at its core. Recent insights into adhesion receptor signaling now propose that integrins, but also cadherins, can centrally control these programs. It is suggested that the two types of adhesion receptors act as sensors to transmit extracellular stimuli in an outside-in mode, to inversely modulate epidermal growth factor receptor signaling and ensure cell survival. Hence, cell-matrix and cell-cell adhesion receptors likely play a more powerful and wide-ranging role than initially anticipated. This Perspective article discusses the relevance of this emerging field for epidermal growth and differentiation, which can be of importance for severe pathologies such as tumorigenesis and invasive metastasis, as well as psoriasis and Pemphigus vulgaris.
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页码:501 / 516
页数:16
相关论文
共 141 条
[1]   beta-catenin is a target for the ubiquitin-proteasome pathway [J].
Aberle, H ;
Bauer, A ;
Stappert, J ;
Kispert, A ;
Kemler, R .
EMBO JOURNAL, 1997, 16 (13) :3797-3804
[2]   FIBRONECTIN INHIBITS THE TERMINAL DIFFERENTIATION OF HUMAN KERATINOCYTES [J].
ADAMS, JC ;
WATT, FM .
NATURE, 1989, 340 (6231) :307-309
[3]   Mice expressing a mutant desmosomal cadherin exhibit abnormalities in desmosomes, proliferation, and epidermal differentiation [J].
Allen, E ;
Yu, QC ;
Fuchs, E .
JOURNAL OF CELL BIOLOGY, 1996, 133 (06) :1367-1382
[4]   Differential regulation of α6β4 integrin by PKC isoforms in murine skin keratinocytes [J].
Alt, A ;
Gartsbein, M ;
Ohba, M ;
Kuroki, T ;
Tennenbaum, T .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2004, 314 (01) :17-23
[5]   AUTOANTIBODIES AGAINST A NOVEL EPITHELIAL CADHERIN IN PEMPHIGUS-VULGARIS, A DISEASE OF CELL-ADHESION [J].
AMAGAI, M ;
KLAUSKOVTUN, V ;
STANLEY, JR .
CELL, 1991, 67 (05) :869-877
[6]   Are desmoglein autoantibodies essential for the immunopathogenesis of pemphigus vulgaris, or just 'witnesses of disease'? [J].
Amagai, M. ;
Ahmed, A. R. ;
Kitajima, Y. ;
Bystryn, J. C. ;
Milner, Y. ;
Gniadecki, R. ;
Hertl, M. ;
Pincelli, C. ;
Fridkis-Hareli, M. ;
Aoyama, Y. ;
Frusic-Zlotkin, M. ;
Mueller, E. ;
David, M. ;
Mimouni, D. ;
Vind-Kezunovic, D. ;
Michel, B. ;
Mahoney, M. ;
Grando, S. .
EXPERIMENTAL DERMATOLOGY, 2006, 15 (10) :815-831
[7]   p120-ctn: A nexus for contextual signaling via Rho GTPases [J].
Anastasiadis, Panos Z. .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2007, 1773 (01) :34-46
[8]   Pemphigus vulgaris IgG causes a rapid depletion of desmoglein 3 (Dsg3) from the Triton X-100 soluble pools, leading to the formation of Dsg3-depleted desmosomes in a human squamous carcinoma cell line, DJM-1 cells [J].
Aoyama, Y ;
Kitajima, Y .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1999, 112 (01) :67-71
[9]   c-Myc activation in transgenic mouse epidermis results in mobilization of stem cells and differentiation of their progeny [J].
Arnold, I ;
Watt, FM .
CURRENT BIOLOGY, 2001, 11 (08) :558-568
[10]  
BAKER J, 1993, J CELL SCI, V104, P415