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    Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/34604

    標題: Crassolide Induces G2/M Cell Cycle Arrest, Apoptosis, and Autophagy in Human Lung Cancer Cells via ROS-Mediated ER Stress Pathways
    作者: Lai, Kuan-Ming
    Wang, Jou-Hsuan
    Lin, Shih-Chao
    Wen, Ya
    Wu, Chao-Liang
    Su, Jui-Hsin
    Chen, Chien-Chin
    Lin, Chi-Chien
    貢獻者: National Chung Hsing University
    Changhua Christian Hospital
    National Chung Hsing University
    National Taiwan Ocean University
    Karolinska Institutet
    National Museum of Marine Biology & Aquarium
    Department of Cosmetic Science, Chia Nan University of Pharmacy & Science
    China Medical University Taiwan
    China Medical University Hospital - Taiwan
    Taichung Veterans General Hospital
    Kaohsiung Medical University
    Asia University Taiwan
    關鍵字: endoplasmic-reticulum stress
    cytotoxic cembranolides
    soft corals
    日期: 2022
    上傳時間: 2023-12-11 14:00:21 (UTC+8)
    出版者: MDPI
    摘要: Crassolide, a cembranoid diterpene extracted from the soft coral Lobophytum crissum, has been proven to possess antioxidant and immunomodulatory properties. In the present study, we assessed the anticancer effects of crassolide on human H460 non-small-cell lung cancer (NSCLC) cells. We found that crassolide exerted cytotoxic effects on H460 cancer cells in vitro, inducing G2/M phase arrest and apoptosis. In addition, in H460 cells exposed to crassolide, the expression of the autophagy-related proteins LC3-II and beclin was increased, while the expression of p62 was decreased. Moreover, inhibiting autophagy with chloroquine (CQ) suppressed the crassolide-induced G2/M arrest and apoptosis of H460 cells. Moreover, we also found that crassolide induced endoplasmic reticulum (ER) stress in lung cancer cells by increasing the expression of ER stress marker proteins and that the crassolide-induced G2/M arrest, apoptosis, and autophagy were markedly attenuated by the ER stress inhibitor 4-phenylbutyric acid (4-PBA). Furthermore, we found that crassolide promoted reactive oxygen species (ROS) production by H460 cells and that the ROS inhibitor N-acetylcysteine (NAC) decreased the crassolide-induced ER stress, G2/M arrest, apoptosis, and autophagy. In conclusion, our findings show that crassolide inhibits NSCLC cell malignant biological behaviors for the first time, suggesting that this effect may be mechanistically achieved by inducing G2/M arrest, apoptosis, and autophagy through ROS accumulation, which activates the ER stress pathway. As a result of our findings, we now have a better understanding of the molecular mechanism underlying the anticancer effect of crassolide, and we believe crassolide might be a candidate for targeted cancer therapy.
    Appears in Collections:[化妝品應用與管理系(所)] 期刊論文

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