Carcinogenesis, Vol 18, 15-21, Copyright © 1997 by Oxford University Press
PR Holden, B McGuire, A Stoler, A Balmain and JD Pitts
Gap junction intercellular communication (GJIC) has been measured in cell
lines that represent different stages of chemically induced mouse skin
carcinogenesis. No significant difference in GJIC, as measured by dye
spread, was found in cultures of normal keratinocyte, papilloma or squamous
carcinoma cell lines. There was no correlation, in this system, between the
presence of a mutant Ha-ras gene and down- regulation of communication.
There was, however, a marked decrease in GJIC (80-90%) on progression from
squamous to spindle carcinoma cells. Measurement of GJIC in somatic cell
hybrids shows that the genetic defect responsible for this down-regulation
is recessive and is common to two independently isolated spindle cell
lines. No abnormalities were found in the spindle cells in expression of
connexin 43, a cell component involved in gap junction formation and
permeability. However, expression of E-cadherin, a cell-cell adhesion
molecule implicated in the process of gap junction formation, was missing
in the spindle carcinoma cells. Introduction of an E-cadherin cDNA into the
spindle cells partially restored junctional communication without causing
any noticeable alterations in cell morphology. During the study a non-
tumourigenic keratinocyte line, a sub-clone of a normal keratinocyte line,
was also found to have a low level of GJIC. However, the defect in this
line was shown, by genetic complementation in somatic cell hybrids, to be
different from that in the spindle carcinoma cell lines. Consistent with
these data, analysis by immunofluorescence shows an abnormal distribution
of connexin 43 in these cells.
ARTICLES
Changes in gap junctional intercellular communication in mouse skin carcinogenesis
The Beatson Institute for Cancer Research, CRC Beatson Laboratories, Bearsden, Glasgow, UK.
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