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.