Connexins and cancer

被引:139
作者
Mesnil, M [1 ]
机构
[1] Univ Poitiers, CNRS UMR 6558, Equipe Commun Jonct, Lab Biomembranes & Signalisat Cellulaire, F-86022 Poitiers, France
关键词
gap junctional intercellular communication; gap junction; connexin; cancer; tumour suppression; cell growth;
D O I
10.1016/S0248-4900(02)00025-4
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The hypothesis, that gap junctional intercellular communication plays a key role in carcinogenesis and more generally in growth control was formulated nearly 40 years ago. From this time, data accumulated, showing that this type of communication is frequently decreased or absent in cells treated with tumor promoting agents, among transformed cells or between transformed/tumor cells and normal cells. This observation has been made on various cell types and whatever their tissue and species origins, by using in vitro and in vivo models. It led to the general assumption that the inhibition of gap junctional intercellular communication may play a role in carcinogenesis at two levels: (1) during tumor promotion by favoring the clonal expansion of initiated cells and (2) after the phenotypic transformation of cells by preventing the diffusion of putative "normalizing" factors between tumor cells and surrounding normal cells. During the past decade, the discovery that gap junction proteins, the connexins (Cx), may act as tumour suppressors, by reverting the phenotype of transformed cells confirmed the idea that their lack of function would be actively involved in carcinogenesis. However, we still do not know precisely what are the molecular processes that gap junctional intercellular communication may regulate and still do have very few data concerning the gap junction situation in human cancers. All these aspects are presented from an historical point of view and discussed below. (C) 2002 Editions scientifiques et medicales Elsevier SAS. All rights reserved.
引用
收藏
页码:493 / 500
页数:8
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