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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 李財坤(Tsai-Kun Li) | |
dc.contributor.author | Po-Chen Kuo | en |
dc.contributor.author | 郭柏辰 | zh_TW |
dc.date.accessioned | 2021-05-13T08:37:37Z | - |
dc.date.available | 2019-08-26 | |
dc.date.available | 2021-05-13T08:37:37Z | - |
dc.date.copyright | 2016-08-26 | |
dc.date.issued | 2016 | |
dc.date.submitted | 2016-07-26 | |
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/3856 | - |
dc.description.abstract | 胃腸道基質瘤(Gastrointestinal stromal tumors,簡稱作GISTs)是在腸胃道中,最常發生的原發性間葉(mesenchyme)瘤;此腫瘤以高度表現KIT受體酪氨酸激酶為特點;大多數(約85%)胃腸道基質瘤帶有KIT基因突變而使KIT持續活化而導致腫瘤的發生;此外,胃腸道基質瘤也會高度表現ETV1轉錄因子;過去認為KIT會與ETV1協同作用而導致胃腸道基質瘤的腫瘤生成。本論文首先藉由在不同的胃腸道基質瘤細胞株進行轉染來探討KIT與ETV1的交互作用與調控機制;並使用非錨定依賴性生長實驗來探討KIT與ETV1對胃腸道基質瘤腫瘤生成的影響。實驗結果顯示,ETV1除了可以對KIT進行正向調控之外,還可以增加胃腸道基質瘤的腫瘤生成能力;然而在具有Imatinib抗藥性的胃腸道基質瘤的細胞中,KIT或許不是ETV1的最主要上游調控因子。本論文的另一目標在於探討微小核醣核酸(miR-193a-3p、miR-296-5p、miR-330-5p、miR-627和miR-1237)是否會對ETV1進行調控進而影響胃腸道基質瘤的腫瘤生成;其實驗方法為在GIST48b細胞株中將上述微小核醣核酸中大量表現後進行非錨定依賴性生長實驗;目前實驗結果顯示,這些微小核醣核酸具有調控ETV1-KIT路徑的作用和影響胃腸道基質瘤的腫瘤生成能力;其中,miR-193a-3p對於胃腸道基質瘤的腫瘤生成最具抑癌潛力。綜上所述,此微小核醣核酸-ETV1-KIT路徑在胃腸道基質瘤的腫瘤生成的調控機制可在未來持續研究探討。 | zh_TW |
dc.description.abstract | Gastrointestinal stromal tumors (GISTs) were the most common primary mesenchymal tumor affecting the gastrointestinal tract. GISTs were characterized by the expression of KIT receptor tyrosine kinase. The majority (~ 85%) of GISTs carried active mutations of KIT gene, which were crucial for GISTs development. In addition, the ETV1 transcription factor was also highly expressed in GISTs. Previously, KIT was thought to cooperate with ETV1 in GIST tumorigenesis. In this thesis, the functional and genetic interactions between KIT and ETV1 were studied by a serious of transfection experiments in different GIST cell lines. The tumorigenesis roles of KIT and ETV1 were also investigated by the anchorage-independent growth assays. The results revealed that ETV1 could positively regulate KIT expression and enhance tumorigenicity in GISTs. Nevertheless, KIT played less role in regulating ETV1 in the Imatinib-resistant GIST cell lines. Another aim of this thesis was to investigate the roles of the microRNAs (miR-193a-3p, miR-296-5p, miR-330-5p, miR-627 and miR-1237) in regulating GIST tumorigenesis by targeting ETV1. The anchorage-independent growth assays were performed after the ectopic expression of these microRNAs in GIST48b cell line. Current results revealed that these microRNAs involved in regulation of the ETV1-KIT axis and GIST tumorigenesis with the miR-193a-3p showed the greatest potential to serve as a tumor suppressor to govern GIST initiation. Together, the regulatory mechanisms of the miR-ETV1-KIT axis in GIST tumorigenesis shall be further investigated. | en |
dc.description.provenance | Made available in DSpace on 2021-05-13T08:37:37Z (GMT). No. of bitstreams: 1 ntu-105-R03445122-1.pdf: 2728292 bytes, checksum: 64c08a1cc37cf73186237f5bb2c97d19 (MD5) Previous issue date: 2016 | en |
dc.description.tableofcontents | 口試委員會審定書 i
誌謝 ii 摘要 iii ABSTRACT iv TABLE OF CONTENTS v CHAPTER 1: INTRODUCTION 1 1. Gastrointestinal stromal tumors 1 1.1 Historic Misdiagnosis of GIST 1 1.2 Epidemiology 1 1.3 Clinical presentations of GIST 2 1.4 Prognostic Factors and Risk Prediction of GIST 2 1.5 Pathological Diagnosis of GIST 3 2. KIT: Molecular Pathogenesis of GIST 3 2.1 KIT proto-oncogene receptor tyrosine kinase 3 2.2 Activation of KIT 4 2.3 Downstream signal transduction pathways of KIT 5 2.4 Physiological role of KIT 5 2.5 The roles of KIT mutations in human diseases 6 2.6 The roles of KIT mutations in GIST 6 2.7 Tyrosine kinase inhibitor therapy for advanced GIST 6 3. ETV1: Molecular Pathogenesis of GIST 7 3.1 ETV1 transcription factor 7 3.2 Physiological role of ETV1 8 3.3 The role of ETV1 in human neoplasms 8 3.4 The role of ETV1 in GISTs 9 4. MicroRNAs 10 4.1 MiRNAs and Tumors 10 4.2 Candidate miRNAs potential to inhibit tumorigenesis of GIST by targeting ETV1 from previous experiments 10 CHAPTER 2: SPECIFIC AIM 11 CHAPTER 3: MATERIALS AND METHODS 12 Cell lines 12 Cell viability assay (MTT assay) 12 Neon transfection system 13 Western blot analysis 13 RNA extraction 14 Reverse transcription polymerase chain reaction (RT-PCR) 14 Colony formation assay 15 Anchorage-independent growth assay (Soft agar assay) 15 CHAPTER 4: RESULTS 16 1. Investigation of the regulatory mechanism between ETV1 and KIT in GISTs 16 1.1 The expression patterns of KIT and ETV1 in the GIST cell lines 16 1.2 Knock down of ETV1 resulted in downregulation of KIT expression 16 1.3 Altering KIT expression did not obviously affect ETV1 expression in the Imatinib-resistant GIST cell lines 17 2. Investigation of the functional roles of ETV1 and KIT in GIST tumorigenesis 18 2.1 The plating efficiency of GIST48b was not influenced by ETV1 or KIT expression 18 2.2 The anchorage-independent growth of GIST48b was positively correlated with ETV1 expression 18 3. Investigation of the functional roles of candidate miRNAs in ETV1-KIT axis and GIST tumorigenesis 19 3.1 Candidate miRNAs predicted to regulate GIST tumorigenesis by targeting ETV1 (from previous experiments) 19 3.2 Several miRNAs inhibited ETV1 activity and downregulated KIT expression in GISTs 20 3.3 The anchorage-independent growth of GISTs were affected by the miRNAs 21 3.4 The re-prediction of ETV1-targeting miRNAs by miRSystem 21 CHAPTER 5: DISCUSSION 23 1. The roles of the ETV1-KIT axis in different GISTs 23 1.1 Previous studies of the KIT-MAPK-ETV1-KIT positive feedback loop in Imatinib-sensitive cell line 23 1.2 Inconsistent results revealed that KIT might played less functions in Imatinib-resistant GISTs 23 1.3 The ETV1-KIT axis was a potential target in treatments of GISTs 25 2. The roles of the candidate miRNAs in ETV1-KIT axis and GIST tumorigenesis 26 2.1 The miR-193a-3p had the greatest potential to inhibit GIST tumorigenesis 26 2.2 The miR-193a-3p had the potential to regulated GIST tumorigenesis by target ETV1 and KIT 26 CHAPTER 6: TABLES AND FIGURES 28 Table 1 Proposed approach for defining risk of aggressive behavior in GISTs 28 Table 2 Basic genetic profile and Imatinib sensitivity of GIST cell lines 29 Table 3 Prediction of regulatory miRNAs targeting ETV1 gene by miRSystem 30 Figure 1 The cell survival curves of the Imatinib-resistant GIST48b cells and the Imatinib-sensitive GIST882 cells under different concentration of Imatinib treatments. 31 Figure 2 Transfection of different GIST cell lines by the Neon transfection system 32 Figure 3 Different GIST cell lines presents with various levels of KIT and ETV1 33 Figure 4 Expression of KIT is reduced after knockdown of ETV1 in two GIST cell lines 34 Figure 5 Expression of KIT doesn’t change obviously after overexpression of ETV1 in GIST48b cells 35 Figure 6 Expression of ETV1 is reduced after knockdown of KIT in GIST882 cells whereas it doesn’t change obviously in GIST48b cells 36 Figure 7 Expression of ETV1 doesn’t change obviously after overexpression of KIT in GIST48b cells 37 Figure 8 Expression of ETV1 doesn’t change obviously after overexpression of KIT with different mutations or splicing forms in GIST62 and GIST48b cells 38 Figure 9 Plating Efficiency is not affected by overexpression of ETV1 or KIT in GIST48b cells 39 Figure 10 Plating Efficiency is not affected by knockdown of ETV1 or KIT in GIST48b cells 40 Figure 11 Anchorage-independent growth of GIST48b cells is increased after overexpression of ETV1 42 Figure 12 Anchorage-independent growth of GIST48b cells is decreased after knockdown of ETV1 44 Figure 13 Previous screening data for miRNAs that might target ETV1 and involve in GIST tumorigenesis 46 Figure 14 Expressions of KIT and ETV1 are decreased after overexpression of several candidate miRNAs 47 Figure 15 Anchorage-independent growth of GIST48b cells is decreased after overexpression of miR-193a-3p, miR-330-5p and miR-627 49 Figure 16 The sequence of miR-193a-3p and its target sites on ETV1 and KIT 50 Figure 17 Model of the roles of miRNAs in regulation of ETV1 and KIT and tumorigenesis of GISTs 51 REFERENCES 52 APPENDIX 67 | |
dc.language.iso | en | |
dc.title | 探討微小核醣核酸−ETV1−KIT之路徑在胃腸道基質瘤中對於腫瘤生成之影響 | zh_TW |
dc.title | Investigation of the miR-ETV1-KIT Axis in the development of Gastrointestinal Stromal Tumors | en |
dc.type | Thesis | |
dc.date.schoolyear | 104-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 賴逸儒(I-Rue Lai),董馨蓮(Shin-Lian Doong) | |
dc.subject.keyword | 胃腸道基質瘤,KIT受體酪氨酸激?,ETV1轉錄因子,微小核醣核酸,腫瘤生成,非錨定依賴性生長, | zh_TW |
dc.subject.keyword | Gastrointestinal stromal tumor,GIST,KIT receptor tyrosine kinase,ETV1 transcription factor,microRNA,anchorage-independent growth,tumorigenesis, | en |
dc.relation.page | 68 | |
dc.identifier.doi | 10.6342/NTU201601168 | |
dc.rights.note | 同意授權(全球公開) | |
dc.date.accepted | 2016-07-27 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 微生物學研究所 | zh_TW |
顯示於系所單位: | 微生物學科所 |
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