Abstract
Induction of apoptosis in transformed fibroblasts by surrounding normal cells has been discussed as a potent early control step in carcinogenesis. According to this hypothesis, tumor progression should require resistance of transformed cells against this TGF-beta-triggered control mechanism. Here we show that Bcl-2, a protein involved in inhibition of apoptosis, can protect transformed cells from induction of apoptosis by surrounding cells. Rather than acting on the transformation process itself, Bcl-2 may thus represent an efficient modulator of carcinogenesis at an intercellular level.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Apoptosis / drug effects*
-
Cell Line
-
Cell Line, Transformed
-
Cell Transformation, Neoplastic / chemically induced
-
Cell Transformation, Neoplastic / metabolism*
-
Cell Transformation, Neoplastic / radiation effects
-
Cells, Cultured / drug effects
-
Cells, Cultured / radiation effects
-
Disease Progression
-
Fibroblasts / drug effects
-
Fibroblasts / metabolism
-
Fibroblasts / radiation effects
-
Mice
-
Mice, Inbred C3H
-
Proto-Oncogene Proteins c-bcl-2 / physiology*
-
Transforming Growth Factor beta / physiology
-
Transforming Growth Factor beta / toxicity
-
Ultraviolet Rays
Substances
-
Proto-Oncogene Proteins c-bcl-2
-
Transforming Growth Factor beta