https://scholars.lib.ntu.edu.tw/handle/123456789/630843
標題: | Oxidative-Stress-Mediated ER Stress Is Involved in Regulating Manoalide-Induced Antiproliferation in Oral Cancer Cells | 作者: | Peng, Sheng-Yao Tang, Jen-Yang Lan, Ting-Hsun Shiau, Jun-Ping Chen, Kuan-Liang JIIANG-HUEI JENG Yen, Ching-Yu Chang, Hsueh-Wei |
關鍵字: | ER expansion; ER stress; aggresome; apoptosis; autophagy; marine sponges; oral cancer | 公開日期: | 16-二月-2023 | 出版社: | MDPI | 卷: | 24 | 期: | 4 | 來源出版物: | International journal of molecular sciences | 摘要: | Manoalide provides preferential antiproliferation of oral cancer but is non-cytotoxic to normal cells by modulating reactive oxygen species (ROS) and apoptosis. Although ROS interplays with endoplasmic reticulum (ER) stress and apoptosis, the influence of ER stress on manoalide-triggered apoptosis has not been reported. The role of ER stress in manoalide-induced preferential antiproliferation and apoptosis was assessed in this study. Manoalide induces a higher ER expansion and aggresome accumulation of oral cancer than normal cells. Generally, manoalide differentially influences higher mRNA and protein expressions of ER-stress-associated genes (PERK, IRE1α, ATF6, and BIP) in oral cancer cells than in normal cells. Subsequently, the contribution of ER stress on manoalide-treated oral cancer cells was further examined. ER stress inducer, thapsigargin, enhances the manoalide-induced antiproliferation, caspase 3/7 activation, and autophagy of oral cancer cells rather than normal cells. Moreover, N-acetylcysteine, an ROS inhibitor, reverses the responses of ER stress, aggresome formation, and the antiproliferation of oral cancer cells. Consequently, the preferential ER stress of manoalide-treated oral cancer cells is crucial for its antiproliferative effect. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/630843 | ISSN: | 16616596 | DOI: | 10.3390/ijms24043987 |
顯示於: | 臨床牙醫學研究所 |
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