NBT-II carcinoma behaviour is not dependent on cell-cell communication through gap junctions

被引:3
作者
Lesueur, F
Mesnil, M
Delouvée, A
Girault, JM
Yamasaki, H
Thiery, JP
Jouanneau, J
机构
[1] Inst Curie, Res Sect, CNRS, UMR 144, F-75248 Paris 05, France
[2] Univ Poitiers, CNRS, Biomembranes & Cell Signaling UMR 6558, F-86022 Poitiers, France
[3] Int Agcy Res Canc, Genet & Canc Susceptibil Unit, F-69372 Lyon, France
关键词
carcinoma; connexin; 43; GJIC; antisense strategy; cell-cell communication; tumour proliferation; community effect;
D O I
10.1016/S0006-291X(02)00451-5
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
To study the mechanism(s) underlying the proliferation of heterogeneous cell populations within a solid turnout, the NBT-II rat bladder carcinoma system was used. It has been first investigated whether the different cell populations are coupled through gap junctions (GJIC). Cells overexpressing the Cx43 were generated to test for any tumour suppressive activity in vivo. To determine whether GJIC is essential for tumour proliferation and the establishment of a cooperative community effect, NBT-II cells that are incompetent for cell coupling were generated. The data report that (i) carcinoma cells expressing or not FGF-I are coupled through GJIC in vitro and in coculture and express the gap junction protein Cx43, (ii) overexpression of Cx43 in these cells does not affect their in vitro coupling capacities and in vivo tumourigenic growth properties, (iii) inhibition of GJIC through antisense strategy has no in vivo obvious consequence on the tumour growth properties of the carcinoma, and (iv) the community effect between two carcinoma cell populations does not critically involve cell coupling through gap junctions. (C) 2002 Elsevier Science (USA). All rights reserved.
引用
收藏
页码:108 / 115
页数:8
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