期刊
PLOS ONE
卷 7, 期 11, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0050607
关键词
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资金
- National Institutes of Health (NIH) [CA106599, RR018733]
- Kentucky Lung Cancer Research Program
- University of Louisville
- NIH [AA018016]
- Commonwealth of Kentucky Research Challenge Trust Fund
While the cytotoxic effects of titanium dioxide (TiO2) nanoparticles have been under intense investigation, the molecular mechanisms of this cytotoxicity remain unknown. Here we investigated the influence of oncogenic transformation and a major apoptotic signaling pathway on cellular responses to TiO2 nanoparticles. Isogenic wild-type (WT) and apoptosis-resistant (Bak(-/-)Bax(-/-)) cell lines with and without tumorigenic transformation were examined. TiO2 nanoparticles preferentially reduced viability of tumorigenic cells in a dose-dependent fashion compared with their untransformed counterparts. Importantly, the elevated cytotoxicity of TiO2 nanoparticles was independent of a major Bak/Bax-dependent apoptosis pathway. Because transformation does not affect cellular fluid-phase endocytosis or nanoparticle uptake, it is likely that the increased cytotoxicity in tumor cells is due to the interaction between TiO2 nanoparticles and the lysosomal compartment. Overall, our data indicate that TiO2 nanoparticles induce cytotoxicity preferentially in transformed cells independent of a major apoptotic signaling pathway.
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