CHEMICAL, ONCOGENE AND GROWTH-FACTOR INHIBITION OF GAP JUNCTIONAL INTERCELLULAR COMMUNICATION - AN INTEGRATIVE HYPOTHESIS OF CARCINOGENESIS

被引:152
|
作者
TROSKO, JE [1 ]
CHANG, CC [1 ]
MADHUKAR, BV [1 ]
KLAUNIG, JE [1 ]
机构
[1] MED COLL OHIO, DEPT PATHOL, TOLEDO, OH 43699 USA
关键词
Cancer cells; Carcinogenesis; Chemicals; Gap junction; Growth factors; Intercellular communication; Oncogene;
D O I
10.1159/000163596
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Most, if not all, cancer cells have some dysfunction in gap-junction-mediated intercellular communication, either because of defects in cell adhesion or inability to have functional gap junctional communication. In addition, most, if not all, tumor-promoting chemicals and conditions down-regulate gap junction function, while some antitumor-promoting chemicals can up-regulate gap junctional communication. Several oncogenes are associated with down-regulation of gap junction function and several hormone and growth regulators, known to be tumor promoters, are also able to down-regulate gap junction function. On the other hand, some tumor suppressor genes have been linked to the up-regulation of gap junctions. Based on these observations, it is hypothesized that, if a progenitor cell is unable to perform gap junctional intercellular communication, normal growth control and cell differentiation would not be possible, thereby favoring the development of malignant neoplasia. © 1990 S. Karger AG, Basel.
引用
收藏
页码:265 / 278
页数:14
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