資料載入中.....
|
請使用永久網址來引用或連結此文件:
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
mitochondria
checkpoints
cdc25c
death |
| 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. |
| 關聯: | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.23, n.10, 5624 |
| 顯示於類別: | [化妝品應用與管理系(所)] 期刊論文
|
文件中的檔案:
| 檔案 |
描述 |
大小 | 格式 | 瀏覽次數 |
|---|
| ijms23105624.pdf | | 13327Kb | Adobe PDF | 45 | 檢視/開啟 | | index.html | | 0Kb | HTML | 85 | 檢視/開啟 |
|
在CNU IR中所有的資料項目都受到原著作權保護.
|
