| Summary: | 碩士 === 國立成功大學 === 細胞生物及解剖學研究所 === 94 === Taxol (paclitaxel) is a potent anticancer agent known to inhibit cell growth and to trigger significant apoptosis in various cancer cells. In clinical therapy, taxol acts as a chemotherapeutic agent against many kinds of head and neck cancers. Although taxol can induce the apoptosis of head and neck cancers, its exact mechanism remains elusive. The exact mechanism of taxol-induced apoptosis in different cancer cell lines is important information that can be used in clinical to select anti cancer drug for chemotherapy of cancer. Herein, the possible mechanism of taxol-induced apoptosis in human head and neck cancer cell line is being investigated. Previous data in our lab have shown that activation of caspase-8, -9, -3, -6, -7, JNK and the cleavage of PARP were involved in taxol-induced OEC-M1 cancer cells apoptosis. Present data illustrated that the phosphorylation of FADD and cleavage of Bid occurred in taxol-treated OEC-M1 cells. Furthermore, SP600125 (JNK inhibitor) cotreated with taxol significantly inhibited JNK phosphorylation and cleavage of caspase-8, -9, -3, -6 and -7. JNK inhibitior also decreased the rate of apoptosis and inhibited the mitochondrial membrane potential change in taxol-treated cells. In conclusion, JNK might contribute to the activation of caspase-8 and the cleavage of Bid, which could cross link the mitochondria pathway in taxol-treated OEC-M1 cells.
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