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dc.contributor.authorXia, Jun
dc.contributor.authorLi, Youjian
dc.contributor.authorYang, Qingling
dc.contributor.authorMei, Chuanzhong
dc.contributor.authorChen, Zhiwen
dc.contributor.authorBao, Bin
dc.contributor.authorAhmad, Aamir
dc.contributor.authorMiele, Lucio
dc.contributor.authorSarkar, Fazlul H
dc.contributor.authorWang, Zhiwei
dc.date.accessioned2013-04-22T13:57:54Z
dc.date.issued2012
dc.identifier.citationXia, Jun, Youjian Li, Qingling Yang, Chuanzhong Mei, Zhiwen Chen, Bin Bao, Aamir Ahmad, Lucio Miele, Fazlul H. Sarkar, and Zhiwei Wang. 2012. Arsenic trioxide inhibits cell growth and induces apoptosis through inactivation of notch signaling pathway in breast cancer. International Journal of Molecular Sciences 13(8): 9627-9641.en_US
dc.identifier.issn1422-0067en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10579107
dc.description.abstractArsenic trioxide has been reported to inhibit cell growth and induce apoptotic cell death in many human cancer cells including breast cancer. However, the precise molecular mechanisms underlying the anti-tumor activity of arsenic trioxide are still largely unknown. In the present study, we assessed the effects of arsenic trioxide on cell viability and apoptosis in breast cancer cells. For mechanistic studies, we used multiple cellular and molecular approaches such as MTT assay, apoptosis ELISA assay, gene transfection, RT-PCR, Western blotting, and invasion assays. For the first time, we found a significant reduction in cell viability in arsenic trioxide-treated cells in a dose-dependent manner, which was consistent with induction of apoptosis and also associated with down-regulation of Notch-1 and its target genes. Taken together, our findings provide evidence showing that the down-regulation of Notch-1 by arsenic trioxide could be an effective approach, to cause down-regulation of Bcl-2, and NF-κB, resulting in the inhibition of cell growth and invasion as well as induction of apoptosis. These results suggest that the anti-tumor activity of arsenic trioxide is in part mediated through a novel mechanism involving inactivation of Notch-1 and its target genes. We also suggest that arsenic trioxide could be further developed as a potential therapeutic agent for the treatment of breast cancer.en_US
dc.language.isoen_USen_US
dc.publisherMolecular Diversity Preservation International (MDPI)en_US
dc.relation.isversionofdoi:10.3390/ijms13089627en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431819/pdf/en_US
dash.licenseLAA
dc.titleArsenic Trioxide Inhibits Cell Growth and Induces Apoptosis through Inactivation of Notch Signaling Pathway in Breast Canceren_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalInternational Journal of Molecular Sciencesen_US
dash.depositing.authorWang, Zhiwei
dc.date.available2013-04-22T13:57:54Z
dc.identifier.doi10.3390/ijms13089627*
dash.contributor.affiliatedWang, Zhiwei


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