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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/80316完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 顧記華(Jih-Hwa Guh) | |
| dc.contributor.author | Yi-Huei Jiang | en |
| dc.contributor.author | 江怡慧 | zh_TW |
| dc.date.accessioned | 2022-11-24T03:04:22Z | - |
| dc.date.available | 2021-08-30 | |
| dc.date.available | 2022-11-24T03:04:22Z | - |
| dc.date.copyright | 2021-08-30 | |
| dc.date.issued | 2021 | |
| dc.date.submitted | 2021-06-28 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/80316 | - |
| dc.description.abstract | "肺癌是全球最常見的惡性腫瘤類型，同時也是死亡率最高的癌症，其中又以非小細胞肺癌（non-small cell lung cancer）佔多數。雖然目前有許多化療藥物及標靶治療，但在台灣非小細胞肺癌的五年存活率仍然低於20%，且大部分的化療藥物會產生嚴重的副作用，因此開發新的治療藥物並且降低副作用是極為重要的。本篇論文發現化合物SPS-7（以三唑為基礎的FTY720衍生物）有效抑制非小細胞肺癌株NCI-H460的生長及增殖。同時發現SPS-7造成MAPK及Akt/mTOR/p70S6K/4EBP1的訊息傳遞減少，其中Akt/mTOR訊息傳遞是調控細胞生長及複製，非小細胞肺癌形成的初期也被報導對Akt/mTOR訊息傳遞具有依賴性。透過myristylated-Akt（持續活化Akt）能逆轉SPS-7對於mTOR/p70S6K/4EBP1及ERK所造成的抑制效果，證實Akt作為mTOR轉譯途徑以及活化ERK重要的上游調控角色，並且大量表現Myr-Akt 也降低SPS-7在細胞生長抑制的效果，代表Akt在NCI-H460細胞為重要的增殖訊息傳遞。SPS-7同時也能活化凋亡蛋白酶（caspase-8, -7, -3），造成sub-G1細胞群體數量增加，引發外源性細胞凋亡。此外，Akt/mTOR訊息傳遞及細胞凋亡（apoptosis）也被發現存在脂筏（lipid raft）上，SPS-7也造成在脂筏上的Akt/mTOR訊息傳遞減少，但透過外加膽固醇能部分回復減少的訊息傳遞。此外，近期的研究發現一些新穎的脂筏型態，例如細胞凋亡訊息傳遞因子富集的脂筏聚集（clusters of apoptotic signaling molecule-enriched rafts, CASMERs），本篇論文也發現SPS-7引起脂筏的重新分布，並聚集細胞凋亡接受體Fas到脂筏形成CASMERs，最終導致外源性細胞凋亡的增加。總結來說，此研究數據顯示SPS-7具有潛力成為治療非小細胞肺癌的藥物，其透過抑制Akt/mTOR訊息傳遞及MAPK訊息途徑，減少細胞增殖，同時影響脂筏的分佈，導致脂筏上的訊息改變，最終產生細胞凋亡。" | zh_TW |
| dc.description.provenance | Made available in DSpace on 2022-11-24T03:04:22Z (GMT). No. of bitstreams: 1 U0001-2306202123410000.pdf: 13205264 bytes, checksum: a02fd98035ea9f49d5591add7735b547 (MD5) Previous issue date: 2021 | en |
| dc.description.tableofcontents | 中文摘要 i Abstract ii List of Abbreviations iv Contents vi List of Figures viii List of Tables ix Aim of the Study 1 Chapter 1: Introduction 4 1.1 Lung cancer 4 1.2 Non-samll cell lung cancer (NSCLC) 4 1.3 FTY720 7 1.4 SPS-7 9 1.5 Apoptosis 9 1.6 PI3K/Akt/mTOR pathway 11 1.7 Lipid raft 12 1.8 MAPK 12 1.9 Autophagy 13 Chapter 2: Materials and Methods 15 2.1 Materials 15 2.2 Methods 16 Chapter 3: Results 24 3.1 Effect of FTY720 and SPS-7 on cell viability and cell proliferation in NCI-H460 cells. 24 3.2 Effect of SPS-7 on cell cycle progression in NCI-H460 cells. 24 3.3 Effect of SPS-7 on cell apoptosis in NCI-H460 cells. 25 3.4 Effect of SPS-7 on Akt/mTOR signaling in NCI-H460 cells. 25 3.5 Effect of SPS-7 on MAPK signaling in NCI-H460 cells. 26 3.6 Localization and meditation of Akt/mTOR signaling in lipid rafts. 26 3.7 Aggregation of Fas/CD95 in lipid rafts. 27 3.8 Effect of SPS-7 on autophagy in NCI-H460 cells. 28 Chapter 4: Discussion 30 Chapter 5: Conclusion 35 Appendices 36 Figures 38 References 55 | |
| dc.language.iso | zh-TW | |
| dc.subject | 三唑類化合物 | zh_TW |
| dc.subject | 脂筏 | zh_TW |
| dc.subject | 非小細胞肺癌 | zh_TW |
| dc.subject | FTY720 | zh_TW |
| dc.subject | Akt | zh_TW |
| dc.subject | 細胞凋亡 | zh_TW |
| dc.subject | Akt | en |
| dc.subject | lipid raft | en |
| dc.subject | apoptosis | en |
| dc.subject | non-small cell lung cancer | en |
| dc.subject | triazole-based compound | en |
| dc.subject | FTY720 | en |
| dc.title | 探討三唑及氨基二醇為基礎的衍生物在人類非小細胞肺癌之抗癌機轉研究 | zh_TW |
| dc.title | Study of Anticancer Mechanism of Triazole-Based Aminodiol Derivative against Human Non-Small Cell Lung Cancer | en |
| dc.date.schoolyear | 109-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 黃聰龍(Hsin-Tsai Liu),許麗卿(Chih-Yang Tseng),蕭哲志,楊家榮 | |
| dc.subject.keyword | FTY720,三唑類化合物,非小細胞肺癌,Akt,細胞凋亡,脂筏, | zh_TW |
| dc.subject.keyword | FTY720,triazole-based compound,non-small cell lung cancer,Akt,apoptosis,lipid raft, | en |
| dc.relation.page | 62 | |
| dc.identifier.doi | 10.6342/NTU202101116 | |
| dc.rights.note | 同意授權(限校園內公開) | |
| dc.date.accepted | 2021-06-28 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 藥學研究所 | zh_TW |
| 顯示於系所單位： | 藥學系 | |
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