Carcinogenesis, Vol 19, 2085-2093, Copyright © 1998 by Oxford University Press
GR Ehring, RJ Antoniono and JL Redpath
Decreased connexin gene expression and loss of the capacity for either
homologous or heterologous intercellular communication has been associated
with neoplastic transformation. We tested the hypothesis that loss of gap
junctional intercellular communication (GJIC) correlates with tumorigenic
potential in the HeLa x skin fibroblast human hybrid cell system. Connexin
gene expression, gap junction function and tumorigenicity were determined
for the non-tumorigenic somatic hybrid cell line (CGL1) and a series of
UVC-induced tumorigenic cell lines derived from CGL1. CGL1 and the parental
skin fibroblasts express connexin43 (alpha1 gap junction gene) mRNA and
protein, form gap junctional plaques and have functional gap junctions.
UVC- irradiation of CGL1 cells produced a cell line (UV12) with an
aggressive tumorigenic phenotype, which lost connexin43 expression as well
as both homologous and heterologous GJIC and was in this respect similar to
HeLa cells. However, the phenotype of UV12 cells exhibited some instability
and revertants to a less aggressive tumorigenic phenotype were isolated.
These cells expressed connexin43 mRNA and protein, and demonstrated
homologous GJIC. Furthermore, cells reconstituted from a tumor derived from
this revertant cell line retained significant connexin43 expression and
homologous GJIC, although they exhibited an aggressive tumorigenic
phenotype. Thus, functional homologous GJIC cannot be dissociated from
tumorigenicity in this system. However, heterologous GJIC between these
same UVC-induced tumorigenic cell lines and normal human skin fibroblasts
was reduced, whereas the non-tumorigenic hybrid cells showed extensive
heterologous GJIC. In summary, re-acquisition of connexin43 expression and
homologous GJIC does not restore the non-tumorigenic phenotype in UVC-
induced tumorigenic HeLa skin fibroblast human hybrid cells. However,
reduction of heterologous GJIC does correlate with tumorigenicity in this
cell system.
ARTICLES
Gap junction expression following UVC-induced neoplastic transformation in human hybrid cell lines
Department of Physiology, College of Medicine, University of California Irvine, 92697, USA. grehring@uci.edu
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