Apigenin Induces Apoptosis through Mitochondrial Dysfunction in U-2 OS Human Osteosarcoma Cells and Inhibits Osteosarcoma Xenograft Tumor Growth in Vivo
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- 作者：Chin-Chung Lin ; Ya-Ju Chuang ; Chien-Chih Yu ; Jai-Sing Yang ; Chi-Cheng Lu ; Jo-Hua Chiang ; Jing-Pin Lin ; Nou-Ying Tang ; An-Cheng Huang ; Jing-Gung Chung
- 刊名：Journal of Agricultural and Food Chemistry
- 出版年：2012
- 出版时间：November 14, 2012
- 年：2012
- 卷：60
- 期：45
- 页码：11395-11402
- 全文大小：483K
- 年卷期：v.60,no.45(November 14, 2012)
- ISSN：1520-5118
文摘
The cytostatic drug from natural products has acted as a chemotherapeutic agent used in treatment of a wide variety of cancers. Apigenin, a type of flavonoid, exhibits anticancer actions, but there is no report to show that apigenin induced apoptosis in osteosarcoma cells. The aim of this study was to investigate the effects of apigenin on U-2 OS human osteosarcoma cells and clarify that the apigenin-induced apoptosis-associated signals. The cytotoxic effects of apigenin were examined by culturing U-2 OS cells with or without apigenin. The percentage of viable cells via PI staining, apoptotic cells, productions of ROS and Ca2+, and the level of mitochondrial membrane potential (螖唯m) were assayed by flow cytometry. The levels of apoptosis-related proteins were measured by immunoblotting. Results indicated that apigenin significantly decreased cell viability. Apigenin effectively induced apoptosis through the activations of caspase-3, -8, -9, and BAX and promoted the release of AIF in U-2 OS cells. In nude mice bearing U-2 OS xenograft tumors, apigenin inhibited tumor growth. In conclusion, apigenin has anticancer properties for induction of cell apoptosis in U-2 OS cells and suppresses the xenograft tumor growth. These findings offer novel information that apigenin possibly possesses anticancer activity in human osteosarcoma.