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https://tkuir.lib.tku.edu.tw/dspace/handle/987654321/118755
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| 題名: | ZnO Nanoparticles Induced Caspase-Dependent Apoptosis in Gingival Squamous Cell Carcinoma through Mitochondrial Dysfunction and p70S6K Signaling Pathway |
| 作者: | 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 |
| 關鍵詞: | zinc oxide nanoparticles;gingival cancer;superoxide;p70S6K pathway |
| 日期: | 2020-02-26 |
| 上傳時間: | 2020-06-02 12:10:16 (UTC+8) |
| 出版者: | MDPI |
| 摘要: | 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. |
| 關聯: | International Journal of Molecular Science 21(5), 1612 |
| DOI: | 10.3390/ijms21051612 |
| 顯示於類別: | [水資源及環境工程學系暨研究所] 期刊論文
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