淡江大學機構典藏:Item 987654321/118755
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    Title: ZnO Nanoparticles Induced Caspase-Dependent Apoptosis in Gingival Squamous Cell Carcinoma through Mitochondrial Dysfunction and p70S6K Signaling Pathway
    Authors: Wang, Shih-Wei;Lee, Chien-Hsing;Lin, Ming-Shen;Chi, Chih-Wen;Chen, Yu-Jen;Wang, Guo-Shou;Liao, Kuang-Wen;Chiu, Li-Pin;Wu, Shu-Hui;Huang, Dong-Ming;Chen, Luke;Shen, Yung-Shuen
    Keywords: zinc oxide nanoparticles;gingival cancer;superoxide;p70S6K pathway
    Date: 2020-02-26
    Issue Date: 2020-06-02 12:10:16 (UTC+8)
    Publisher: MDPI
    Abstract: Zinc oxide nanoparticles (ZnO-NPs) are increasingly used in sunscreens, food additives,
    pigments, rubber manufacture, and electronic materials. Several studies have shown that ZnO-NPs
    inhibit cell growth and induce apoptosis by the production of oxidative stress in a variety of
    human cancer cells. However, the anti-cancer property and molecular mechanism of ZnO-NPs in
    human gingival squamous cell carcinoma (GSCC) are not fully understood. In this study, we found
    that ZnO-NPs induced growth inhibition of GSCC (Ca9-22 and OECM-1 cells), but no damage in
    human normal keratinocytes (HaCaT cells) and gingival fibroblasts (HGF-1 cells). ZnO-NPs caused
    apoptotic cell death of GSCC in a concentration-dependent manner by the quantitative assessment of
    oligonucleosomalDNAfragmentation. Flow cytometric analysis of cell cycle progression revealed that
    sub-G1 phase accumulation was dramatically induced by ZnO-NPs. In addition, ZnO-NPs increased
    the intracellular reactive oxygen species and specifically superoxide levels, and also decreased the
    mitochondrial membrane potential. ZnO-NPs further activated apoptotic cell death via the caspase
    cascades. Importantly, anti-oxidant and caspase inhibitor clearly prevented ZnO-NP-induced cell
    Int. J. Mol. Sci. 2020, 21, 1612; doi:10.3390/ijms21051612 www.mdpi.com/journal/ijms
    Int. J. Mol. Sci. 2020, 21, 1612 2 of 16
    death, indicating the fact that superoxide-induced mitochondrial dysfunction is associated with the
    ZnO-NP-mediated caspase-dependent apoptosis in human GSCC. Moreover, ZnO-NPs significantly
    inhibited the phosphorylation of ribosomal protein S6 kinase (p70S6K kinase). In a corollary in vivo
    study, our results demonstrated that ZnO-NPs possessed an anti-cancer eect in a zebrafish xenograft
    model. Collectively, these results suggest that ZnO-NPs induce apoptosis through the mitochondrial
    oxidative damage and p70S6K signaling pathway in human GSCC. The present study may provide
    an experimental basis for ZnO-NPs to be considered as a promising novel anti-tumor agent for the
    treatment of gingival cancer.
    Relation: International Journal of Molecular Science 21(5), 1612
    DOI: 10.3390/ijms21051612
    Appears in Collections:[Graduate Institute & Department of Water Resources and Environmental Engineering] Journal Article

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