Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.biomaterials.2011.07.036
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dc.titleThe role of the tumor suppressor p53 pathway in the cellular DNA damage response to zinc oxide nanoparticles
dc.contributor.authorNg, K.W.
dc.contributor.authorKhoo, S.P.K.
dc.contributor.authorHeng, B.C.
dc.contributor.authorSetyawati, M.I.
dc.contributor.authorTan, E.C.
dc.contributor.authorZhao, X.
dc.contributor.authorXiong, S.
dc.contributor.authorFang, W.
dc.contributor.authorLeong, D.T.
dc.contributor.authorLoo, J.S.C.
dc.date.accessioned2014-10-09T07:04:23Z
dc.date.available2014-10-09T07:04:23Z
dc.date.issued2011-11
dc.identifier.citationNg, K.W., Khoo, S.P.K., Heng, B.C., Setyawati, M.I., Tan, E.C., Zhao, X., Xiong, S., Fang, W., Leong, D.T., Loo, J.S.C. (2011-11). The role of the tumor suppressor p53 pathway in the cellular DNA damage response to zinc oxide nanoparticles. Biomaterials 32 (32) : 8218-8225. ScholarBank@NUS Repository. https://doi.org/10.1016/j.biomaterials.2011.07.036
dc.identifier.issn01429612
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/90360
dc.description.abstractIn this paper, we explored how ZnO nanoparticles cross-interact with a critical tumor suppressive pathway centered around p53, which is one of the most important known tumor suppressors that protects cells from developing cancer phenotypes through its control over major pathways like apoptosis, senescence and cell cycle progression. We showed that the p53 pathway was activated in BJ cells (skin fibroblasts) upon ZnO nanoparticles treatment with a concomitant decrease in cell numbers. This suggests that cellular responses like apoptosis in the presence of ZnO nanoparticles require p53 as the molecular master switch towards programmed cell death. This also suggests that in cells without robust p53, protective response can be tipped towards carcinogenesis when stimulated by DNA damage inducing agents like ZnO nanoparticles. We observed this precarious tendency in the same BJ cells with p53 knocked down using endogeneous expressing shRNA. These p53 knocked down BJ cells became more resistant to ZnO nanoparticles induced cell death and increased cell progression. Collectively, our results suggest that cellular response towards specific nanoparticle induced cell toxicity and carcinogenesis is not only dependent on specific nanoparticle properties but also (perhaps more importantly) the endogenous genetic, transcriptomic and proteomic landscape of the target cells. © 2011 Elsevier Ltd.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.biomaterials.2011.07.036
dc.sourceScopus
dc.subjectDNA damage
dc.subjectGenotoxicology
dc.subjectNanoparticles
dc.subjectNanotoxicology
dc.subjectP53
dc.subjectZinc oxide
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.contributor.departmentCHEMICAL & BIOMOLECULAR ENGINEERING
dc.description.doi10.1016/j.biomaterials.2011.07.036
dc.description.sourcetitleBiomaterials
dc.description.volume32
dc.description.issue32
dc.description.page8218-8225
dc.description.codenBIMAD
dc.identifier.isiut000295241200018
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