| Summary: | 碩士 === 國立東華大學 === 生命科學系 === 99 === The prostate cancer is one of the most common diseases for men and it becomes seriously with the age. In Asian area, the percentage and the death rate of the prostate cancer is increasing year by year for recent years. Taiwanofungus camphorates,also known as Antrodia camphorate (AC), is a kind of medical fungus only found in Taiwan. A lot of previous studies also confirmed that AC can be used for anticancer. According to studies that showed the extracts of AC fruiting body can make tumors be controlled or perished, but it’s effects for the prostate cancer cells were not fully understood. In this study, AC ethanol crude extracts (ACCE) and AC Column Chromatography extracts that named CFK4 and CFK6 were used to investigate that if AC fruiting body can make the prostate cancer cells, LNCaP and PC-3, be controlled. In this study, MTT assay showed that the cell survival rate decreased depending on the increase of dose, with ACCE、CFK4 and CFK6 were investigated on 24hr incubation. Both two tested prostate cancer were more sensitive to CFK6. This study showed that the IC50 of LNCaP and PC-3 were 10.57 μg/ml and 5.42 μg/ml. The results also showed that cellular morphological changes and cell shrinkage and the turn over of the Phosphatidylserine ( PS ) of Cell membrane when the disposal time of CFK6 was increased. By using PI staining, the data showed that the SubG1 of cell cycle was increased in prostate cancer cell, LNCaP and PC-3, treated by CFK6. DNA fragmentation analysis also confirmed that CFK6 could cause a apoptosis effect for both cell lines. According to the above experiment results, CFK6 made the two prostate cancer cell lines move toward apoptosis. Finally the assay about caspase activity and Western blot showed that LNCaP and PC-3 cells treated by increasing CFK6 could up regulate caspase-3, caspase-8, caspase-9 and the Bax ,but down regulate in Bcl-2 protein expression and caspase-7 was not changed. With the increasing concentration of CFK6, p53 protein in LNCaP and PC-3 also increased. Collectively, we showed CFK6 induced apoptosis through the regulation of FasL, p53, caspase-8, caspase-9, caspase-3, and the mitochondria pathway : Bax/Bcl-2 and cytochrome-c.
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