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| Title: | 松杉靈芝甲醇萃取物誘發人類表皮癌細胞細胞凋亡 |
| Other Titles: | Ganoderma tsugae methanol extracts could induce apoptosis in human epidermoid A431 cell |
| Authors: | 黃逸民;Huang, Ii-ming |
| Contributors: | 淡江大學化學學系碩士班
莊子超;Chuang, Tzu-chao |
| Keywords: | 癌症;細胞凋亡;EGFR;松杉靈芝;cancer;apoptosis;EGFR,;Ganoderma tsugae |
| Date: | 2007 |
| Issue Date: | 2010-01-11 02:36:35 (UTC+8) |
| Abstract: | 在亞洲國家中，靈芝是一種用來藥用和養生的菌類。近年來文獻指出靈芝具有免疫修飾 (immunomodulatory) 和抗腫瘤的能力 (anti-tumor) 。另一方面而言，表皮生長因子受體 (Epidermal Growth Factor Receptor, EGFR) 是在許多癌症中具有過度表現或是基因突變的一種原致癌基因，其中發生在皮膚癌、大腸癌、乳癌、腦癌和子宮頸癌等等。我們發現在松杉靈芝甲醇萃取高濃度 (1 mg/ml) 下，對人類表皮癌 A431 細胞不只有明顯的細胞毒性，且也會誘發細胞凋亡。本論文中，我們證實松杉靈芝甲醇萃取物誘發EGFR過度表現的人類表皮癌A431細胞凋亡可能的路徑。實驗結果中發現，松杉靈芝甲醇萃取物能夠有效的降低 A431 細胞 EGFR 蛋白表現並且也發現也能降低Akt活性。這顯示松杉靈芝甲醇萃取物誘發A431細胞凋亡和降低 EGFR 具有緊密的關係。更近一步探討，也發現靈芝甲醇萃取物能夠誘發粒腺體釋放 cytochrome c 並活化下游 caspase 3 和抑制 PARP 活性，最後也發現松杉靈芝甲醇萃取物能夠降低A431的抗細胞凋亡蛋白 (Bcl-2, Bcl-xL) 表現。因此松杉靈芝甲醇萃取物對於EGFR過度表現A431 細胞不只降低 EGFR 蛋白表現也抑制其下游訊號傳遞，而抑制其增生作用，最後誘發由 caspase 所引起的細胞凋亡。
Ganoderma (Lingzhi), an oriental fungus, has been widely used as a medical drug or health-promotion product in Asian countries. Lingzhi have been demonstrated to possess immunomodulatory and anti-tumor activities. On the other hand, the Epidermal Growth Factor Receptor (EGFR) is frequently amplified, overexpressed, or mutated in many cancers, including skin, colon, lung, breast, head and neck cancer. We have investigated, at high doses (>1 mg/ml), the methanol extracts from the Ganoderma tsugae
(G. tsugae) could be cytotoxic through induction of apoptosis. In the present study, we examined the effect of G. tsugae extract on apoptotic biochemical events in EGFR-overexpressing human epidermoid carcinoma A431 cells. G. tsugae extracts treatment could down-regulate the EGFR protein level and cause the de-phosphorylation/inactivation of constitutively active AKT. This data suggest that G. tsugae extracts could induce apoptosis might through downregulation of EGFR in A431 cells. Furthermore,
G. tsugae extracts also could induce release of cytochrome c accompanied by activation of caspase-3 and PARP cleavage. Finally, treatment of A431 cells with G. tsugae extracts could down-regulate the expression of inhibitors of apoptosis protein, such as Bcl-2 and Bcl-xL. Taken together, our finding suggest that G. tsugae extracts could down-regulate EGFR protein level and its downstream signaling pathway in EGFR-overexpressing human epidermoid carcinoma A431 cells leading to the inhibition of
proliferationand induction of caspase-dependent apoptosis. |
| Appears in Collections: | [化學學系暨研究所] 學位論文
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