β-catenin signaling in fibroproliferative disease

被引:99
作者
Bowley, Erin
O'Gorman, David B.
Gan, Bing Siang
机构
[1] Univ Western Ontario, Hand & Upper Limb Ctr, Cell & Mol Biol Lab, London, ON N6A 3K7, Canada
[2] Univ Western Ontario, Dept Surg, Lawson Hlth Res Inst, London, ON N6A 3K7, Canada
[3] Univ Western Ontario, Dept Physiol, Lawson Hlth Res Inst, London, ON N6A 3K7, Canada
[4] Univ Western Ontario, Dept Pharmacol, Lawson Hlth Res Inst, London, ON N6A 3K7, Canada
[5] Univ Western Ontario, Dept Med Biophys, Lawson Hlth Res Inst, London, ON N6A 3K7, Canada
基金
加拿大健康研究院;
关键词
Wnt/beta-catenin signaling; fibroproliferative disorders; Dupuytren's contracture; wound healing; hypertrophic scarring;
D O I
10.1016/j.jss.2006.07.026
中图分类号
R61 [外科手术学];
学科分类号
摘要
Background. beta-catenin has been historically recognized as both an intermediate in the "canonical Wnt signaling pathway" and as a component of functional adherens junctions. Materials and methods. Cellular accumulation of beta-catenin levels can result in transactivation of gene transcription and cellular proliferation during normal cellular and disease development. Recent evidence has identified A-catenin in an additional role as a component of cutaneous wound healing. Results. This finding is in keeping with previous observations that post-translational modifications of 13-catenin that are associated with its cytoplasmic accumulation are frequently observed in fibroproliferative diseases with characteristics of dysregulated wound healing. These diseases include hypertrophic scar formation, aggressive fibromatoses, Lederhose disease, and Dupuytren's contracture (DC). Conclusions. While its precise roles in disease initiation and progression remain to be explored, this review highlights our current knowledge of P-catenin regulation and describes some potential upstream mediators of 13-catenin accumulation and signaling in fibroproliferative disease. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:141 / 150
页数:10
相关论文
共 113 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]   COMPARATIVE EFFECTS OF GROWTH-FACTORS ON FIBROBLASTS OF DUPUYTRENS TISSUE AND NORMAL PALMAR FASCIA [J].
ALIOTO, RJ ;
ROSIER, RN ;
BURTON, RI ;
PUZAS, JE .
JOURNAL OF HAND SURGERY-AMERICAN VOLUME, 1994, 19A (03) :442-452
[3]  
Alman BA, 1997, AM J PATHOL, V151, P329
[4]   Aggressive fibromatosis (desmoid tumor) is a monoclonal disorder [J].
Alman, BA ;
Pajerski, ME ;
DiazCano, S ;
Corboy, K ;
Wolfe, HJ .
DIAGNOSTIC MOLECULAR PATHOLOGY, 1997, 6 (02) :98-101
[5]   Axin-mediated CKI phosphorylation of β-catenin at Ser 45:: a molecular switch for the Wnt pathway [J].
Amit, S ;
Hatzubai, A ;
Birman, Y ;
Andersen, JS ;
Ben-Shushan, E ;
Mann, M ;
Ben-Neriah, Y ;
Alkalay, I .
GENES & DEVELOPMENT, 2002, 16 (09) :1066-1076
[6]   Making sense of latent TGFβ activation [J].
Annes, JP ;
Munger, JS ;
Rifkin, DB .
JOURNAL OF CELL SCIENCE, 2003, 116 (02) :217-224
[7]   Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response [J].
Ashcroft, GS ;
Yang, X ;
Glick, AB ;
Weinstein, M ;
Letterio, JJ ;
Mizel, DE ;
Anzano, M ;
Greenwell-Wild, T ;
Wahl, SM ;
Deng, CX ;
Roberts, AB .
NATURE CELL BIOLOGY, 1999, 1 (05) :260-266
[8]   Insulin-like growth factor binding protein-6: The "forgotten" binding protein? [J].
Bach, LA .
HORMONE AND METABOLIC RESEARCH, 1999, 31 (2-3) :226-234
[9]   Functional interaction of beta-catenin with the transcription factor LEF-1 [J].
Behrens, J ;
vonKries, JP ;
Kuhl, M ;
Bruhn, L ;
Wedlich, D ;
Grosschedl, R ;
Birchmeier, W .
NATURE, 1996, 382 (6592) :638-642
[10]   LOSS OF EPITHELIAL DIFFERENTIATION AND GAIN OF INVASIVENESS CORRELATES WITH TYROSINE PHOSPHORYLATION OF THE E-CADHERIN BETA-CATENIN COMPLEX IN CELLS TRANSFORMED WITH A TEMPERATURE-SENSITIVE V-SRC GENE [J].
BEHRENS, J ;
VAKAET, L ;
FRIIS, R ;
WINTERHAGER, E ;
VANROY, F ;
MAREEL, MM ;
BIRCHMEIER, W .
JOURNAL OF CELL BIOLOGY, 1993, 120 (03) :757-766