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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 林欽塘(Chin-Tarng Lin) | |
| dc.contributor.author | Ya-Chun Chang | en |
| dc.contributor.author | 張雅淳 | zh_TW |
| dc.date.accessioned | 2021-06-15T11:48:15Z | - |
| dc.date.available | 2019-08-26 | |
| dc.date.copyright | 2016-08-26 | |
| dc.date.issued | 2016 | |
| dc.date.submitted | 2016-08-12 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/49785 | - |
| dc.description.abstract | 鼻咽癌是種好發於鼻咽部的癌症 ，其發生的族群以東南亞國家為主例如：香港、新加坡、及中國沿海地區(廣東、福建)，此外非洲的人民也不少人得此病，世界衛生組織將鼻咽癌分為三類，第一類為：未分化的鱗狀上皮細胞癌、第二類為：非角質化細胞癌、第三類為：未分化細胞癌，鼻咽癌的致癌因素包括：病毒感染、飲食習慣、遺傳、環境..等。而其中最為大家所耳熟能詳的是EBV病毒感染，研究雖然顯示患有第一類未分化鱗狀上皮細胞癌的病人約有百分之96機率，可在他們的血液中測到EBV病毒的DNA，但根據許多報導顯示，我們有理由相信EBV不是導致鼻咽癌發生的主因，而是促使鼻咽癌增生的發生，本論文之主要研究目的，是想找出導致鼻咽癌發生的相關基因，首先我們使用cDNA 微陣列分析去比較正常鼻咽黏膜上皮細胞與鼻咽癌的表現量，再由定量聚合酶連鎖反應(Quantitative RT-PCR)、西方點墨法(Western Blotting)的研究發現chemokine (CC motif) of ligand28 (CCL28)基因，在鼻咽癌細胞中有明顯增加，而且在進而研究CCL28在鼻咽癌中扮演的角色及其造成的影響時，我們發現Interferon alpha-inducible protein 6 (IFI6)基因在鼻咽癌細胞中也有明顯增加的表現量，尤其是在TW06N1細胞上，因此我們決定深入研究IFI6基因在鼻咽癌中扮演的角色以及其功能，首先我們訂購IFI6之shRNA ，將其感染到鼻咽癌細胞中，建立一個knockdown的系統，使鼻咽癌細胞中的IFI6表現量下降，之後我們去做一連串的細胞功能分析(functional analysis)，發現鼻咽癌細胞不管在爬行能力、侵襲力、以
及細胞增長能力方面都有明顯下降的趨勢，而另外在細胞凋亡現象方面，我們也發現其凋亡現象增加，與此同時，我們也另外建立了另一個shCCL28之細胞株，一樣是用shRNA病毒去感染鼻咽癌細胞使其細胞中的CCL28的表現量下降，我們發現當CCL28的表現量下降時，IFI6的表現量也跟著下降，我們相信CCL28與IFI6之間可能存在一個調節的關係。在異種移植的鼻咽癌腫瘤 (NPC xenografts)長於NOD-SCID之老鼠的實驗中發現以抑制IFI6基因表現的shRNA所轉染的鼻咽癌細胞在NOD-SCID老鼠體內長到第六週時，腫瘤重量比控制組小了百分之七十八，在免疫染色與組織病理分析時發現抑制IFI6基因表達能減緩異種移植的腫瘤細胞生長並伴隨著嚴重的細胞凋亡。基於以上這些實驗結果 我們相信IFI6基因在未來很有潛力成為新的鼻咽癌治療標的。 | zh_TW |
| dc.description.abstract | Nasopharyngeal carcinoma (NPC) is the most common cancer originating in the nasopharynx. It is one of the most common cancers among East Asia (Taiwan,Hong Kong , Singapore,southern China) and Africa . The World Health Organization (WHO) criteria for nasopharyngeal cancer has been published. They are Type 1 .Differentiated squamous cell carcinoma , Type 2 .Non keratinizing carcinoma,Type 3. Undifferentiated carcinoma. Nasopharyngeal carcinoma is caused by a combination of factors including viral infection , environmental influences, and heredity. The viral influence is associated with infection with Epstein-Barr virus , EBV DNA was detectable in the blood plasma samples of 96% of patients with non-keratinizing NPC. The purpose of this research was to find out the genes associated with NPC pathogenesis . First , we use cDNA microarray analysis of mRNA expression between NPC cell lines and normal nasal mucosal epithelial cells,CCL28 gene expression was found significantly increased in NPC cell lines by quantitative RT-PCR and IHC. In our previous studied of the function of CCL28 gene in NPC , we found that Interferon alpha-inducible protein 6 ( IFI6 ) was also significantly increased in NPC , especially in NPC-TWO6N1. To further identify the relationship between CCL28 and IFI6 , we performed some investigation to clarify this condition. We found the CCL28 could affect the gene expression of IFI6 . In order to study the role of IFI6 in the molecular pathogenesis of NPC and its functions，we transfect shRNA in NPC cell to construct stable shIFI6 NPC cell lines as a knockdown system . we found the tumor cells could be down-regulated to express IFI6 mRNA and protein about 40-50% , We also found that when IFI6 was down-regulated , the ability of cell migration , invasion ,proliferation were decreased . On the other hand , the apoptosis of NPC was promoted. We also knocked down CCL28 by using shRNA to create a shCCL28 system and found that when CCL28 was down-regulated , the protein expression of IFI6 was decreased . However , when IFI6 knockdown , the gene expression of CCL28 was not significantly changed.
In vivo , we have injected shIFI6 NPC cell line to NOD-SCID mice for 6 weeks , the weight of tumor diminished about 78% and tumor size decreased about 55% after 6 weeks , accompanied by necrosis and apoptosis in the NPC-TW06N1 xenografts treated with IFI6 shRNA histopathologically. These novel findings of the functional role of IFI6 may have a potential implication in molecular target therapy for NPC. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T11:48:15Z (GMT). No. of bitstreams: 1 ntu-105-R01444011-1.pdf: 5021364 bytes, checksum: 995936cfe037fe0e38e3bbe1d963e359 (MD5) Previous issue date: 2016 | en |
| dc.description.tableofcontents | 目錄 Table of Contents
口試委員審定書 ii 致謝 Acknowledgement iii 中文摘要 v Abstract vii List of Figures xi List of Tables xiii Introduction 1 Nasopharyngeal carcinoma (NPC) 1 EtiologyofNPC…………………………………………………………………….3 Molecular Biomarkers and prognostic factorsofNPC………………………………………………………………………4 Interferon-inducible protein6(IFI6)……………………………………………………………………...7 Chemokine (C-C motif) ligand 28 (CCL28) 8 Materials and Methods 12 1. Cell culture 12 2. Extraction of RNA and Preparation of cDNA 13 3. Quantitative real-time PCR (qRT-PCR) 14 4. Statistical analysis of qRT-PCR results 15 5. Immunohistochemical staining 15 6. Western blotting. 17 7. Mini-plasmid purification 17 8. Amplification and Extraction of plasmids 18 9. Establishment of stable shIFI6 NPC cell lines by lentiviral vector system……………………………………………………………………………..19 10. MTT Assay 20 11. Scratch wound healing assay 20 12. Transwell migration assay 21 13. Invasion assay 21 14. Caspase-3 Fluorometric Assay 22 15. In vivo assay of xenograft growth 23 Results 24 IFI6 gene expression in NNM and NPC tumor cell lines 24 Establishment of the stable shIFI6 transfected NPC cell line . 24 IFI6 protein expression in NPC biopsy specimens………………………………..24 Functional analysis of IFI6 gene expression. 25 IFI6 influences the expressions of Caspase3 , Caspase9 and PARP in NPC cell lines to prevent apoptosis. 26 DMEM deprivation induced an apoptosis response in shIFI6 NPC-TW06N1 and NPC-TW01N1 cell lines………………………………………………………………………………………………………… 27 Functional analysis of IFI6 in SCID mice bearing NPC xenografts…………………………………………………………………………27 Figures 29 Discussion 52 Tables 56 References 58 List of Figures Figure 1: The IFI6 mRNA expression in NNM and NPC cell lines.. 29 Figure 2: Expression of IFI6 protein in NPC cell lines………………………………………………. …………………………………...30 Figure 3 :40 NPC patients’ biopsy specimens were examined by IFI6 immunostaining……………………………………………………………………….31 Figure 4: The expression of IFI6 protein in shIFI6 infected NPC –TW06N1. 32 Figure 5:. Effect of IFI6 knockdown on NPC cell proliferation……………………………………………………………………………33 Figure 6: Effect of IFI6 knockdown on NPC line migration.. 34 Figure 7: Effect of IFI6 knockdown on other NPC line migration. 36 Figure 8: Effect of invasion ability in IFI6-knockdown NPC-TW06N1 37 Figure 9: Effect of IFI6 knockdown on Caspase3 and Caspase9 and PARP protein levels by Western blotting…………………………………………………………………………………38 Figure10.To determine the increased enzymatic activity of the Caspase-3 class of proteases in apoptotic cells by fluorometricreaction…………………………………………………………………40 Figure11: DMEM deprivation triggers apoptosis in NPC cell line cells ……………………………………………………………………………………41 Figure 12: DMEM deprivation induce apoptosis activation in NPC cell lines…………………………………………...43 Figure 13: In vivo study of shIFI6-transfected NPC-TW06N1 cells…………………………………………………………………………………….45 Figure14:SCID mice bearing NPC IFI6-knockdown xenografts showing decrease of xenograft sizes and weight…………………………………………………………………………46 Figure 15: Decrease in the gene expression of IFI6 in NPC –TW06N1 from SCID mice xenografts…………………………………………………………………………….47 Figure 16:Immunohistochemical staining of IFI6 in the SCID mice bearing the IFI6 by lentiviral-infected NPC –TW06N1 xenograft……………………………………..............................................................48 Figure 17: Histopathological morphology of the lentiviral-infected NPC –TW06N1 xenograft in SCID mice……………………………………………………………………………………49 Figure 18:The expression of CCL28 mRNA in shIFI6 infected NPC-TW06N1……………………………………………………….50 Figure19:Decrease of IFI6 gene expression in CCL28 knockdown cells……………………………………………………………………………………51 List of Tables Table 1: The primers used to quantitative RT-PCR (qRT-PCR) 56 Table 2: Map of shIFI6, shRNA(-)control and positive control 57 | |
| dc.language.iso | en | |
| dc.subject | 鼻咽癌 | zh_TW |
| dc.subject | IFI6 | zh_TW |
| dc.subject | IFI6之體內外功能分析 | zh_TW |
| dc.subject | 腫瘤發生 | zh_TW |
| dc.subject | CCL28 | zh_TW |
| dc.subject | CCL28 C-C motif chemokine ligand 28(CCL28) | en |
| dc.subject | NPC | en |
| dc.subject | Interferon alpha inducible protein 6 (IFI6) | en |
| dc.subject | Functional analysis of IFI6 in vitro and in vivo | en |
| dc.subject | Tumorigenesis | en |
| dc.title | IFI6 基因在鼻咽癌腫瘤生長所扮演之角色 | zh_TW |
| dc.title | The role of IFI6 gene in nasopharyngeal carcinoma tumorigenesis | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 104-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 吳漢忠(Han-Chung Wu),黃祥博(Hsiang-Po Huang),余明俊(Ming-Jiun Yu) | |
| dc.subject.keyword | 鼻咽癌,腫瘤發生,IFI6,CCL28,IFI6之體內外功能分析, | zh_TW |
| dc.subject.keyword | NPC,Tumorigenesis,Interferon alpha inducible protein 6 (IFI6),CCL28 C-C motif chemokine ligand 28(CCL28),Functional analysis of IFI6 in vitro and in vivo, | en |
| dc.relation.page | 63 | |
| dc.identifier.doi | 10.6342/NTU201602481 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2016-08-12 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 病理學研究所 | zh_TW |
| 顯示於系所單位： | 病理學科所 | |
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