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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/86119完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 蔡孟勳(Mong-Hsun Tsai) | |
| dc.contributor.author | Cheng-Sheng Hsieh | en |
| dc.contributor.author | 謝正陞 | zh_TW |
| dc.date.accessioned | 2023-03-19T23:37:44Z | - |
| dc.date.copyright | 2022-09-30 | |
| dc.date.issued | 2022 | |
| dc.date.submitted | 2022-09-28 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/86119 | - |
| dc.description.abstract | 根據政府歷年統計資料顯示，從70年代開始至今癌症是台灣十大死因之首且癌症發生數連年增加，因此目前癌症發生最新統計資料顯示，和西元2018年相比，西元2019年台灣罹癌個數增加最多的是肺癌，且不論在台灣男性以及在台灣女性肺癌癌症發生數位居前三，此外根據最新癌症死亡數統計指出在西元2021年死亡率最高的癌症是肺癌。然而有些癌症好發於台灣男性，在西元2019年十大癌症發生率性別比差異最大的癌症為食道癌，男性罹患食道癌的機率為女性的15倍。雖然已經有許多研究探討肺癌以及食道癌發生之相關細胞訊號途徑，但是癌症細胞訊號途徑調控很複雜，所以本研究會分別探討CD36以及miR-548ba對肺癌以及食道癌細胞癌化之機制。 實驗室先前已經針對肺癌患者進行研究指出相較於正常肺細胞，CD36低表現量可能在肺癌中扮演重要角色，因此本研究探討CD36低表現量於肺癌生長之影響及機制。首先我們發現CD36基因靜默(Silencing)會抑制CL1-0增生能力(Proliferation)，然而CD36大量表現(Overexpression)不會改變CL1-5的增生能力，但CD36大量表現會抑制H1299的增生能力。在細胞遷移能力實驗當中，使用Transwell發現CD36基因靜默會促進CL1-0遷移能力(Migration)，然而CD36大量表現不會改變CL1-5以及H1299的遷移能力。在細胞凋亡實驗(Cell Apoptosis Assay)當中，CD36基因靜默會降低CL1-0死亡速率，然而CD36大量表現不會改變CL1-5的死亡速率。最後CD36基因靜默會減少CL1-0吞噬之葡萄糖量以及抑制醣解作用(Glycolysis)活性。 除了基因之外，許多研究也指出小分子核醣核酸(microRNA, miRNA)在各種人類癌症中也扮演重要的角色。因此實驗室先前透過次世代定序(Next-Generation Sequencing, NGS)以及即時定量聚合酶連鎖反應(Real-Time Quantitative Polymerase Chain Reaction, QPCR)驗證後發現相較於正常食道細胞，miR-548ba高表現量可能在食道癌中扮演重要角色，因此本研究探討miR-548ba高表現量於食道癌生長之影響及機制。由實驗結果發現miR-548ba大量表現會促進CE81T的增生能力以及增加CE81T細胞群落數目，但不會改變CE81T遷移能力。接著使用預測miRNA目標基因的軟體以及即時定量聚合酶連鎖反應驗證的發現，MOB1B可能是miR-548ba的目標基因，然而MOB1B是否是miR-548ba的直接目標基因仍需後續實驗驗證。 綜合來看，首先CD36在不同肺癌細胞中所造成之細胞生理功能的影響也不同，此外miR-548ba會促進CE81T細胞增生能力，期望透過本研究能提供後人新的研究方向以找出新的肺癌以及食道癌致癌機制。 | zh_TW |
| dc.description.abstract | According to the statistics released by government in the past few years, cancer is the majority of dead reason from 1980s to present in Taiwan. Moreover, the cancer incidence is increasing year after year. Based on the latest statistics of cancer incidence and cancer death released by the Health Promotion Administration in 2019 and 2021 respectively, lung cancer ranked the top three cancer incidence and cancer death in both gender in Taiwan. Additionally, the esophageal cancer incidence in male was fifteen times as much as the esophageal cancer incidence in female. Although most of cancer research focus on lung and esophageal carcinogenesis related cell signaling, the regulation of cancer cell signaling is complex. Thus, in this study, I would focus on the function of CD36 and miR-548ba in lung and esophageal carcinogenesis respectively. In our lab, previous study found that compared with normal lung cells, CD36 low expression may play an important role in lung cancer. Therefore, we investigated the regulatory mechanism of CD36 low expression in lung cancer. First, we found that CD36 silencing inhibited CL1-0 proliferation, whereas CD36 overexpression did not alter CL1-5 proliferation, but CD36 overexpression inhibited H1299 proliferation. Using Transwell, we found that CD36 silencing promoted CL1-0 migration, but CD36 overexpression did not change CL1-5 and H1299 migration. In cell apoptosis assays, CD36 silencing reduced the death rate of CL1-0, whereas CD36 overexpression did not alter the death rate of CL1-5. Finally, CD36 silencing reduced the amount of glucose consumption and inhibited glycolysis activity in CL1-0. Except for genes, many studies had also found that microRNAs (miRNAs) also play important roles in various human cancers. Therefore, in our lab previously found that the high expression of miR-548ba may play an important role in esophageal cancer compared with normal esophageal cells by next-generation sequencing and real-time quantitative polymerase chain reaction. Therefore, we investigated the regulatory mechanism of miR-548ba high expression in esophageal cancer. First, it was found that miR-548ba overexpression promoted CE81T proliferation and increases CE81T colony number, but did not change CE81T migration. Then, using the software for predicting miRNA target genes and the verification by real-time quantitative polymerase chain reaction and found that MOB1B may be the target gene of miR-548ba, but whether MOB1B is the direct target gene of miR-548ba still needs to be verified by subsequent experiments. Overall, my study indicated that CD36 had diverse effects on the physiological functions in different lung cancer cells, and miR-548ba could promote CE81T proliferation. Therefore, it is hoped that it can provide new aspects for researchers to find new lung and esophageal carcinogenesis mechanism in this study. | en |
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| dc.description.tableofcontents | 目錄 致謝 i 摘要 ii Abstract iv 目錄 vii 圖目錄 x 表目錄 xi 1.前言 1 1.1台灣肺癌及食道癌現況以及其介紹 1 1.2高通量技術介紹以及其應用 2 1.2.1去氧核醣核酸微陣列介紹及應用 2 1.2.2次世代定序介紹以及應用 5 1.2.3高通量技術挑選基因之策略以及後續分析 7 1.3基因在癌症中所扮演的角色 8 1.3.1 CD36在癌症中所扮演的腳色 8 1.3.2小分子核醣核酸介紹 9 1.3.3小分子核醣核酸在癌症所扮演的角色 9 1.3.4小分子核醣核酸在食道癌所扮演的角色 10 2.基本原理以及目的 11 3.材料與方法 12 3.1培養液配置 12 3.1.1 DMEM 12 3.1.2 RPMI 1640 12 3.2磷酸鹽緩衝生理食鹽水配置 12 3.3細胞培養 12 3.3.1人類胚胎腎臟細胞(HEK293T) 13 3.3.2人類肺癌細胞(CL1-0、CL1-5、H1299) 13 3.3.3人類食道癌細胞(KYSE70、KYSE410) 14 3.3.4人類食道癌細胞(CE81T、CE81T 1-4) 14 3.4目標質體製備 15 3.5慢病毒製備 15 3.6慢病毒感染 15 3.7小分子核醣核酸轉染 16 3.8核醣核酸萃取 16 3.9反轉錄聚合酶連鎖反應 17 3.9.1基因 17 3.9.2小分子核醣核酸 17 3.10即時定量聚合酶連鎖反應 17 3.10.1基因 18 3.10.2小分子核醣核酸 18 3.11蛋白質萃取 18 3.12西方墨點法 18 3.12.1十二烷基硫酸鈉聚丙烯醯胺凝膠電泳配置 19 3.12.2跑膠 19 3.12.3轉漬 19 3.12.4免疫染色 20 3.13細胞增生實驗 20 3.14細胞遷移實驗 20 3.15細胞凋亡實驗 21 3.16細胞群落形成實驗 21 3.17細胞葡萄糖吞噬實驗 21 3.18統計方法 21 4.結果 23 4.1偵測CD36在不同肺癌細胞之表現量 23 4.2在CL1-0以及CL1-5改變CD36核醣核酸以及蛋白質表現量 23 4.3探討在不同肺癌細胞中CD36對細胞增生能力以及死亡速率的影響 24 4.4探討在不同肺癌細胞中CD36對細胞遷移能力的影響 25 4.5探討CD36對CL1-0葡萄糖吞噬以及醣解作用活性的影響 25 4.6偵測miR-548ba在不同食道癌細胞之表現量 25 4.7在不同食道癌細胞改變miR-548ba核醣核酸表現量 26 4.8探討在不同食道癌細胞中miR-548ba對細胞增生能力的影響 26 4.9探討miR-548ba對CE81T細胞遷移能力的影響 26 4.10探討miR-548ba可能的目標基因 26 5.討論 28 5.1探討CD36基因靜默會促進CL1-0遷移能力，但CD36大量表現不會改變CL1-5遷移能力的原因 28 5.2探討CD36低表現量於肺癌扮演重要角色的原因 28 5.3探討CD36對癌症醣解作用的影響 29 5.4探討在食道癌LIFR不是miR-548ba直接目標基因的原因 29 6.結論 31 圖 32 表 44 7.參考資料 48 圖目錄 圖一、使用即時定量聚合酶連鎖反應偵測不同肺癌細胞CD36相對內生性表現量，且以CL1-0 CD36內生性表現量為基準。 32 圖二、改變CL1-0以及CL1-5 CD36表現量。 33 圖三、CD36對CL1-0、CL1-5以及H1299細胞增生能力以及死亡速率的造成不同影響。 34 圖四、CD36對CL1-0、CL1-5以及H1299細胞遷移能力造成不同影響。 35 圖五、CD36對CL1-0葡萄糖吞噬以及醣解作用活性影響。 36 圖六、使用即時定量聚合酶連鎖反應偵測不同食道癌細胞miR-548ba內生性表現量。 37 圖七、改變KYSE70、KYSE410、CE81T以及CE81T 1-4 miR-548ba核醣核酸表現量。 38 圖八、miR-548ba對KYSE70、KYSE410、CE81T以及CE81T 1-4細胞增生能力影響。 39 圖九、miR-548ba對CE81T細胞遷移能力影響。 40 圖十、使用即時定量聚合酶連鎖反應偵測miR-548ba可能的目標基因。 43 表目錄 表一、進行小分子核醣核酸反轉錄聚合酶連鎖反應所使用之相關引子。 44 表二、進行基因即時定量聚合酶連鎖反應所使用之相關引子。 45 表三、進行小分子核醣核酸即時定量聚合酶連鎖反應所使用之相關引子。 47 | |
| dc.language.iso | zh-TW | |
| dc.title | 研究癌細胞中細胞訊息傳遞路徑之調控：探討CD36在肺癌的機制以及miR-548ba在食道癌的機制 | zh_TW |
| dc.title | To study the mechanism of cell signaling in cancer: CD36 in lung cancer and miR-548ba in esophageal cancer | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 110-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 賴亮全(Liang-Chuan Lai),陳立涵(Li-Han Chen) | |
| dc.subject.keyword | 肺癌,食道癌,CD36,miR-548ba,MOB1B,細胞增生,細胞遷移, | zh_TW |
| dc.subject.keyword | Lung cancer,Esophageal cancer,CD36,miR-548ba,MOB1B,Cell proliferation,Cell migration, | en |
| dc.relation.page | 55 | |
| dc.identifier.doi | 10.6342/NTU202203990 | |
| dc.rights.note | 同意授權(全球公開) | |
| dc.date.accepted | 2022-09-29 | |
| dc.contributor.author-college | 生物資源暨農學院 | zh_TW |
| dc.contributor.author-dept | 生物科技研究所 | zh_TW |
| dc.date.embargo-lift | 2022-09-30 | - |
| 顯示於系所單位： | 生物科技研究所 | |
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