科研之友
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摘要
Objective: Classical chondrosarcoma has poor sensitivity to chemotherapy and radiotherapy, and surgical resection is the only effective treatment. Therefore, development of a novel adjuvant therapy is required. In vitro and in vivo studies have found that apigenin, a type of flavonoid, has anti-tumor activity in various malignancies. The effects of apigenin on human chondrosarcoma and the mechanisms underlying these effects remain unknown. Methods: Here we used different concentration of Apigenin to treat chondrosarcoma cells. Cell viability, Clone formation, Cell cycle, typical apoptotic morphological changes were identified by optical microscopy, Hoechst staining, and transmission electron microscopy. The early and total apoptotic rate was estimated by flow cytometry. Results: We found here apigenin inhibits chondrosarcoma cell proliferation by inducing G2/M phase arrest and inhibiting colony formation. Apigenin treatment induced mitochondrial apoptosis of chondrosarcoma cells by regulating the expression of the Bcl-2 family and activating the Caspase cascade. Exposure to apigenin induced marked ROS generation, reduced the mitochondrial membrane potential, and created an imbalance in intracellular calcium concentration in sw1353 cells. Conclusion: We consider ROS generation to be the major mechanism of apoptosis induction by apigenin. In vivo, apigenin suppressed tumor growth in a mouse xenograft model. Taken together, these results suggest that apigenin exhibits anti-tumor efficacy against chondrosarcoma in vitro and in vivo. Apigenin inhibits proliferation and induces mitochondrial apoptosis via ROS generation in human chondrosarcoma cells. Thus, apigenin is a promising novel adjuvant agent for chondrosarcoma therapy.
