Carcinogenesis, Vol 18, 259-264, Copyright © 1997 by Oxford University Press
J Panse, ML Hipp and G Bauer
The ability of neighbouring normal cells to inhibit proliferation of
transformed cells is regarded as the classical mode of intercellular
control of potential tumour cells. This mechanism, however, only controls
the pool size of transformed cells, but does not impair their survival. We
have recently shown that cells transformed by biological agents are subject
to a novel control system: transforming growth factor beta (TGF-beta)
induces normal cells to release factors that mediate apoptosis specifically
in transformed cells. Here we show that cells transformed by chemical
carcinogens are also subject to this dominant control mechanism. The number
of foci induced by methylcholanthrene, N-methyl-N'-nitro-N-nitrosoguanidine
or quercetin was significantly reduced when the cultures were treated with
TGF-beta. Established lines of chemically transformed cells proved to be
sensitive to induction of apoptosis by neighbouring normal cells in the
presence of TGF-beta. This finding demonstrates that sensitivity to
induction of apoptosis is a general feature of transformed cells,
irrespective of the transforming agent. It is particularly relevant for
chemical carcinogenesis. As transformed cells were shown to trigger
induction of their own apoptosis, the acquisition of resistance to this
process may be a central regulatory step in carcinogenesis in vitro and
possibly also in vivo. This study may help to elucidate mechanisms that
protect transformed cells at an early stage of tumour progression that has
until now not been the focus of investigation.
ARTICLES
Fibroblasts transformed by chemical carcinogens are sensitive to intercellular induction of apoptosis: implications for the control of oncogenesis
Abteilung Virologie, Institut fur Medizinische Mikrobiologie und Hygiene, Universitat Freiburg, Germany.
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