Bleomycin, a widely used anti-tumor agent, is well-known to cause singleand
double-strand breaks in cellular DNA in vivo and in vitro leading finally to genomic
instability of damaged cells. Bleomycin causes an increase of reactive oxygen species,
resulting in oxidative stress and pulmonary fibrosis. Further, bleomycin induces
apoptosis and senescence in epithelial as well as non-epithelial cells of the lung.
Caveolin-1 is a scaffold protein of caveolae, which are particularly abundant in alveolar
epithelial type I cells, in endothelial and smooth muscle cells, and in fibroblasts of lung
tissue. Caveolin-1 directly interacts with signaling molecules and effects diverse
signaling pathways regulating cell proliferation, apoptosis, differentiation, migration
and growth.
In this review we discuss aspects of bleomycin resistance. We summarize recent data
about the effects of bleomycin in terms of lung cell biology and emphasize that
bleomycin-induced injury of lung cells is accompanied by altered expression levels of
caveolin-1. Caveolin-1 is involved in bleomycin-induced apoptosis and senescence of
normal and lung cancer cells. Investigating the role of caveolin-1 may provide new
tools for therapeutic interventions in lung disease and for the understanding of tumor
biology.
Keywords: Apoptosis, bleomycin, caveolin-1, lung cancer, pulmonary fibrosis,
resistance, senescence.