| Summary: | 碩士 === 臺北醫學大學 === 醫學研究所 === 96 === Our previous studies have demonstrated that TSDH could induce cell cycle arrest in G1 phase and cell apoptosis through mitochondrial pathway in human breast cancer. In addition, other study also demonstrated that TSDH induced reactive oxygen species production through depletion of glutathione, and resulted in apoptosis of human hepatoma cells. However, whether TSDH can induce apoptosis through ER (endoplasmic reticulum) stress pathway remains to be examined. In this study, we found that TSDH significantly decreased the proliferation by MTT assay and induced apoptosis by DNA fragmentation and flow cytometry assays in human prostate cancer cells DU145. TSDH was able to induce ER stress, including up-regulation of glucose regulation protein 78 (GRP78), GADD153 (CHOP) and inducing phosphorylation of eIF???? and JNK, and increase XBP1 mRNA splicing form in DU145 cells. In addition, TSDH activated apoptotic relative proteins, including PARP, caspase 9, and caspase 3. The results suggested that TSDH could induce prostate cancer cells apoptosis via induction of ER stress and unfold protein response, and might have therapeutic potential for prostate cancer.
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