Joining S100 proteins and migration: for better or for worse, in sickness and in health

被引:149
作者
Gross, Stephane R. [1 ]
Connie Goh Then Sin [1 ]
Barraclough, Roger [2 ]
Rudland, Philip S. [2 ]
机构
[1] Aston Univ, Sch Life & Hlth Sci, Birmingham B4 7ET, W Midlands, England
[2] Univ Liverpool, Inst Integrat Biol, Liverpool L69 7ZB, Merseyside, England
基金
英国医学研究理事会;
关键词
S100; proteins; Migration/motility; Cancer; Invasion; Cytoskeleton; Receptor; CALCIUM-BINDING PROTEIN; GLYCATION END-PRODUCTS; SQUAMOUS-CELL CARCINOMA; EPITHELIAL-MESENCHYMAL TRANSITION; METASTASIS-ASSOCIATED PROTEIN; FIBROBLAST GROWTH-FACTOR; PANCREATIC-CANCER CELLS; IN-VITRO; PSORIASIN S100A7; RNA INTERFERENCE;
D O I
10.1007/s00018-013-1400-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The vast diversity of S100 proteins has demonstrated a multitude of biological correlations with cell growth, cell differentiation and cell survival in numerous physiological and pathological conditions in all cells of the body. This review summarises some of the reported regulatory functions of S100 proteins (namely S100A1, S100A2, S100A4, S100A6, S100A7, S100A8/S100A9, S100A10, S100A11, S100A12, S100B and S100P) on cellular migration and invasion, established in both culture and animal model systems and the possible mechanisms that have been proposed to be responsible. These mechanisms involve intracellular events and components of the cytoskeletal organisation (actin/myosin filaments, intermediate filaments and microtubules) as well as extracellular signalling at different cell surface receptors (RAGE and integrins). Finally, we shall attempt to demonstrate how aberrant expression of the S100 proteins may lead to pathological events and human disorders and furthermore provide a rationale to possibly explain why the expression of some of the S100 proteins (mainly S100A4 and S100P) has led to conflicting results on motility, depending on the cells used.
引用
收藏
页码:1551 / 1579
页数:29
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