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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 周綠蘋 | |
| dc.contributor.author | Ying-Chu Liao | en |
| dc.contributor.author | 廖瑩竹 | zh_TW |
| dc.date.accessioned | 2021-06-13T04:15:32Z | - |
| dc.date.available | 2016-10-05 | |
| dc.date.copyright | 2011-10-05 | |
| dc.date.issued | 2011 | |
| dc.date.submitted | 2011-07-27 | |
| dc.identifier.citation | 1. Kelley, J.R. and J.M. Duggan, Gastric cancer epidemiology and risk factors. Journal of Clinical Epidemiology, 2003. 56(1): p. 1-9.
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/32785 | - |
| dc.description.abstract | Gastric cancer is the most common malignancy of the gastrointestinal tract in East Asian populations. Although the pathogenic factors involved in gastric carcinogenesis are thought to be multifactorial, infection with Helicobacter pylori (H.pylori) seems to be a main risk factor for the development of gastric cancer nowadays. The significant role of H. pylori on gastrointestinal tract diseases has been proposed, but the detailed mechanism/molecular pathway remains unclear, especially the correlations to miRNAs. MiRNAs are endogenous, small noncoding RNAs, which function by base pairing with the 3’- untranslated region (3’UTR) of target messenger RNAs, thereby regulating as high as 30% of all protein-coding genes expression. One of miRNAs, miR-21, is overexpressed in most tumor types, and acts as an “oncomiR” by targeting many tumor suppressor genes related to numerous cancer-related phenotypes.
To reveal the correlation between H.pylori infection and miR-21, we first verified that miR-21 is overexpressed aberrantly in AGS cells caused by H. pylori infection using qRT-PCR. Following we developed a miR-21 stable cell line which constantly expresses higher level of miR-21 than the mock one. Furthermore, we searched the potential targets of miR-21 using 2-Dimentional Electrophoresis (2DE) to compare the differences proteome between miR-21 stable cell line and mock, following identified the potential target proteins by LC-MS/MS. Continuing analyzed these identified and predicted proteins with IPA (Ingenuity Pathway Analysis) bioinformatics approach, we observed that these potential targets, such as tumor suppressor PDCD4 (programmed cell death 4), may involve in proliferation and apoptosis pathways. We further verified the potential target PDCD4 and its relevant pathway by luciferase reporter assay combined mutagenesis assay, finding that PDCD4 indeed down-regulated directly by miR-21 overexpression as well as H.pylori infection in AGS cells. According to MTT assay, cell proliferation rate is decreased by PDCD4 overexpression which correlates to its tumor suppressor role. Therefore, we concluded that PDCD4 is down-regulated by miR-21 overexpression and may lead to increased cell proliferation triggered by H.pylori infection in AGS cells. | en |
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| dc.description.tableofcontents | 目次
謝誌 I 摘要 II ABSTRACT IV 縮寫 VI 第一章 導論 - 1 - 第一節胃癌與幽門螺旋桿菌 - 1 - 1.1胃癌的發生與幽門螺旋桿菌之關係 - 1 - 1.2幽門螺旋桿菌之形態與特徵及流行病學調查 - 2 - 1.3幽門螺旋桿菌的致病因子及宿主反應 - 3 - 第二節 微核醣核酸 (MIRNAS) - 5 - 2.1 miRNAs之生合成路徑及其功能 - 5 - 2.2 微核醣核酸與癌症之關係 - 7 - 2.3 微核醣核酸21 (miR-21) 所扮演的致癌角色 - 8 - 第三節 研究動機 - 9 - 第二章 材料 - 10 - 第一節 幽門螺旋桿菌菌株 - 10 - 第二節 胃腺癌細胞及載體 - 10 - 2.1胃腺癌上皮細胞 - 10 - 2.2 穩定表現miR-21 及只帶有載體 (mock) 之AGS 穩定細胞株 - 10 - 2.3 大量表現miR-21之重組質體 (pSilencer 4.1-CMV-miR-21) - 10 - 第三節 儀器及裝置 - 10 - 第四節 大腸桿菌及質體 - 12 - 第五節 酵素 - 12 - 第六節 抗體 - 12 - 第七節 試劑組與藥品 - 13 - 第八節 軟體與資料庫 - 14 - 第三章 實驗方法 - 15 - 第一節 幽門螺旋桿菌的培養 - 15 - 第二節 胃腺癌細胞的培養 - 15 - 2.1 培養基 (medium) 的配置 - 15 - 2.2 細胞的培養 - 15 - 2.3 細胞的計數 - 16 - 第三節 幽門螺旋桿菌感染胃腺癌細胞 - 16 - 3.1 細胞的準備 (plating) - 16 - 3.2 幽門螺旋桿菌感染胃腺癌細胞 - 16 - 3.3 幽門螺旋桿菌的收取 - 16 - 第四節 定量反轉錄聚合酶連鎖反應 (QRT-PCR) - 17 - 4.1 細胞RNA萃取 - 17 - 4.2 miRNAs反轉錄反應 (reverse transcription, RT) - 17 - 4.3 定量聚合酶鏈鎖反應 (real-time polymerase chain reaction, Q-PCR) - 18 - 第五節 蛋白質分析法 - 19 - 5.1 蛋白質濃度測定 (BCA protein assay) - 19 - 5.2 十二烷基磺酸鈉-聚丙烯醯胺膠體電泳分析 (SDS-PAGE) - 19 - 5.3 西方墨點法 (Western blotting) - 21 - 第六節 質體轉染 (TRANSFECTION) - 22 - 第七節 二維電泳分析 - 23 - 7.1 樣本處理 - 23 - 7.2第一維膠片 (IPG strip) 重新水合化 - 23 - 7.3 第一維等電點展開 (isoelectric focusing, IEF) - 24 - 7.4 第二維電泳分析 (SDS-PAGE) - 24 - 7.5 染色與退染 - 25 - 第八節 膠體原位酵素切割及蛋白質鑑定 - 25 - 第九節 報導基因表現分析 (LUCIFERASE REPORT ASSAY) - 25 - 9.1細胞準備及轉染 - 25 - 9.2 Luciferase reagent buffer配置 - 26 - 9.3 Luciferase活性偵測 - 26 - 第十節 重組蛋白之建立 - 26 - 第十一節 細胞生存能力試驗 (MTT ASSAY) - 28 - 11.1 MTT reagent 配置 - 28 - 11.2 細胞準備 - 28 - 11.3 MTT 活性偵測 - 29 - 第四章 結果 - 30 - 第一節 幽門螺旋桿菌感染影響宿主細胞MIR-21表現量 - 30 - 第二節 MIR-21之目標基因及相關致癌路徑 - 31 - 2.1 miR-21 Stable cell line之確立 - 31 - 2.2 二維電泳分析鑑定 miR-21所影響之差異表現蛋白 - 31 - 2.3 軟體預測分析miR-21之標的基因 - 32 - 2.4 miR-21目標基因所影響路徑之資料庫分析 - 35 - 第三節 確認MIR-21目標基因PROGRAMMED CELL DEATH 4 - 36 - 3.1 利用Luciferase assay確認PDCD4為miR-21之目標基因 - 36 - 3.2 幽門螺旋桿菌感染促進miR-21表現而抑制PDCD4報導基因表現 - 37 - 第四節 MIR-21及PDCD4之功能性分析 - 37 - 4.1 大量表現miR-21促進細胞生長；大量表現PDCD4抑制細胞生長 - 38 - 4.2同時表現PDCD4 3’UTR-wild type及miR-21 回復其生長情形 - 39 - 第五節 幽門螺旋桿菌與PDCD4之關係 - 39 - 第五章 討論 - 41 - 第一節 實驗方法學討論 - 41 - 1.1二維電泳分析法的優點與限制 - 41 - 1.2軟體預測之優點與限制 - 41 - 1.3用蛋白體學分析miRNAs的優缺點 - 41 - 第二節 幽門螺旋桿菌與其他MIRNAS之關連性 - 42 - 第三節 MIR-21大量表現所影響其他差異性表現蛋白 - 42 - 3.1 miR-21大量表現後，表現量上升的蛋白質 - 43 - 3.2 miRNAs新功能，促進基因表現 - 43 - 第四節 MIR-21與PDCD4其他致癌機轉 - 44 - 4.1 PDCD4其他抑癌功能 - 44 - 4.2 PDCD4如何抑制細胞增生? - 44 - 第五節 幽門螺旋桿菌與MIR-21之關連性討論 - 45 - 第六節 幽門螺旋桿菌與PDCD4之關連性討論 - 45 - 第七節 MIR-21其他可能目標基因與幽門螺旋桿菌之關係 - 46 - 7.1 幽門螺旋桿菌感染與PDCD4、RECK mRNA表現量之關係 - 46 - 7.2 幽門螺旋桿菌感染與可能miR-21目標基因蛋白表現量之關係 - 46 - 第八節 結語與未來展望 - 47 - 8.1 幽門螺旋桿菌致癌機轉 - 47 - 8.2 未來工作與願景 - 48 - 第六章 參考文獻 - 49 - 圖表 - 56 - 附錄 - 76 - | |
| dc.language.iso | zh-TW | |
| dc.subject | PDCD4 | zh_TW |
| dc.subject | 胃癌 | zh_TW |
| dc.subject | 幽門螺旋桿菌 | zh_TW |
| dc.subject | 微核醣核酸 | zh_TW |
| dc.subject | 微核醣核酸21 | zh_TW |
| dc.subject | miRNAs | en |
| dc.subject | PDCD4 | en |
| dc.subject | miR-21 | en |
| dc.subject | Gastric cancer | en |
| dc.subject | Helicobacter pylori | en |
| dc.title | 利用蛋白體學技術鑑定受幽門螺旋桿菌感染之人類胃腺癌上皮細胞中微核醣核酸21之標的 | zh_TW |
| dc.title | Proteomics Approach to Identify miR-21 Targets in Helicobacter pylori-infected AGS Cells | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 99-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 俞松良,詹世鵬,蕭朱杏 | |
| dc.subject.keyword | 胃癌,幽門螺旋桿菌,微核醣核酸,微核醣核酸21,PDCD4, | zh_TW |
| dc.subject.keyword | Gastric cancer,Helicobacter pylori,miRNAs,miR-21,PDCD4, | en |
| dc.relation.page | 102 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2011-07-28 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 生物化學暨分子生物學研究所 | zh_TW |
| 顯示於系所單位： | 生物化學暨分子生物學科研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-100-1.pdf 未授權公開取用 | 4.12 MB | Adobe PDF |
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