INVOLVEMENT OF GAP-JUNCTIONS IN TUMORIGENESIS - TRANSFECTION OF TUMOR-CELLS WITH CONNEXIN-32 CDNA RETARDS GROWTH-INVIVO

被引:231
作者
EGHBALI, B
KESSLER, JA
REID, LM
ROY, C
SPRAY, DC
机构
[1] YESHIVA UNIV ALBERT EINSTEIN COLL MED, DEPT NEUROSCI, 1410 PELHAM PKWY S, BRONX, NY 10461 USA
[2] YESHIVA UNIV ALBERT EINSTEIN COLL MED, DEPT NEUROL, BRONX, NY 10461 USA
[3] YESHIVA UNIV ALBERT EINSTEIN COLL MED, DEPT MOLEC PHARMACOL, BRONX, NY 10461 USA
关键词
GROWTH CONTROL; MESSENGER RNA; INTERCELLULAR COMMUNICATION; ION CHANNELS; ELECTRICAL COUPLING;
D O I
10.1073/pnas.88.23.10701
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Gap junction channels provide a pathway for exchange of ions and small molecules between coupled cells, and this exchange is believed to be critical for normal tissue growth and development. As a test for a role of gap junction-mediated intercellular communication in control of cell growth, we have compared growth rates of communication-deficient human tumor cells (SKHep1) with clones stably transfected with cDNA encoding the rat liver gap junction protein connexin 32. In culture, growth rates for parental and transfected clones were similar. However, when sizes of tumors were evaluated following injection of these clones into athymic nude mice, growth rates for two well-coupled clones were significantly lower than for communication-deficient or poorly coupled clones. This study demonstrates that growth rate of these tumor cells in situ is negatively correlated with strength of intercellular communication.
引用
收藏
页码:10701 / 10705
页数:5
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