Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/95489
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dc.contributor.authorHuang, Shingzh_TW
dc.contributor.authorChueh, Pin Juzh_TW
dc.contributor.authorLin, Yun-Weizh_TW
dc.contributor.authorShih, Tung-Shengzh_TW
dc.contributor.authorChuang, Show-Meizh_TW
dc.contributor.author莊秀美zh_TW
dc.date2009-12-01-
dc.date.accessioned2018-10-05T03:21:33Z-
dc.date.available2018-10-05T03:21:33Z-
dc.identifier.urihttp://hdl.handle.net/11455/95489-
dc.description.abstractTitanium dioxide (TiO2) nano-particles (<100 nm in diameter) have been of interest in a wide range of applications, such as in cosmetics and pharmaceuticals because of their low toxicity. However, recent studies have shown that TiO2 nano-particles (nano-TiO2) induce cytotoxicity and genotoxicity in various lines of cultured cells as well as tumorigenesis in animal models. The biological roles of nano-TiO2 are shown to be controversial and no comprehensive study paradigm has been developed to investigate their molecular mechanisms. In this study, we showed that short-term exposure to nano-TiO2 enhanced cell proliferation, survival, ERK signaling activation and ROS production in cultured fibroblast cells. Moreover, long-term exposure to nano-TiO2 not only increased cell survival and growth on soft agar but also the numbers of multinucleated cells and micronucleus (MN) as suggested in confocal microscopy analysis. Cell cycle phase analysis showed G2/M delay and slower cell division in long-term exposed cells. Most importantly, long-term TiO2 exposure remarkably affected mitotic progression at anaphase and telophase leading to aberrant multipolar spindles and chromatin alignment/segregation. Moreover, PLK1 was demonstrated as the target for nano-TiO2 in the regulation of mitotic progression and exit. Notably, a higher fraction of sub-G1 phase population appeared in TiO2-exposed cells after releasing from G2/M synchronization. Our results demonstrate that long-term exposure to nano-TiO2 disturbs cell cycle progression and duplicated genome segregation, leading to chromosomal instability and cell transformation.zh_TW
dc.language.isoenzh_TW
dc.publisherTOXICOLOGY AND APPLIED PHARMACOLOGYzh_TW
dc.relationToxicology and applied pharmacology, Volume 241, Issue 2, Page(s) 182-94.zh_TW
dc.relation.urihttps://www.sciencedirect.com/science/article/pii/S0041008X09003494?via%3Dihubzh_TW
dc.subjectAnimalszh_TW
dc.subjectCell Cycle Proteinszh_TW
dc.subjectCell Proliferationzh_TW
dc.subjectCell Survivalzh_TW
dc.subjectCell Transformation, Neoplasticzh_TW
dc.subjectCytotoxinszh_TW
dc.subjectDNA Damagezh_TW
dc.subjectDose-Response Relationship, Drugzh_TW
dc.subjectDrug Administration Schedulezh_TW
dc.subjectExtracellular Signal-Regulated MAP Kinaseszh_TW
dc.subjectMicezh_TW
dc.subjectMitosiszh_TW
dc.subjectNIH 3T3 Cellszh_TW
dc.subjectNanoparticleszh_TW
dc.subjectProtein-Serine-Threonine Kinaseszh_TW
dc.subjectProto-Oncogene Proteinszh_TW
dc.subjectReactive Oxygen Specieszh_TW
dc.subjectTitaniumzh_TW
dc.subjectChromosome Segregationzh_TW
dc.titleDisturbed mitotic progression and genome segregation are involved in cell transformation mediated by nano-TiO2 long-term exposurezh_TW
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/j.taap.2009.08.013zh_TW
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.fulltextwith fulltext-
item.languageiso639-1en-
item.grantfulltextrestricted-
Appears in Collections:生物醫學研究所
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