Interference of bcl-2 with intercellular control of carcinogenesis.
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.
Jürgensmeier
J M
JM
Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, Germany.
Bauer
G
G
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D002461:Cell Line, Transformed; D002471:Cell Transformation, Neoplastic / Q000139:chemically induced / Q000378:metabolism* / Q000528:radiation effects; D002478:Cells, Cultured / Q000187:drug effects / Q000528:radiation effects; D018450:Disease Progression; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D051379:Mice; D008809:Mice, Inbred C3H; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000502:physiology / Q000633:toxicity; D014466:Ultraviolet Rays
D019253:Proto-Oncogene Proteins c-bcl-2; D016212:Transforming Growth Factor beta