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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/82323完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 陳瑞華(Ruey-Hwa Chen) | |
| dc.contributor.author | Ru-Yin Jian | en |
| dc.contributor.author | 簡茹因 | zh_TW |
| dc.date.accessioned | 2022-11-25T07:29:13Z | - |
| dc.date.available | 2024-08-08 | |
| dc.date.copyright | 2021-11-19 | |
| dc.date.issued | 2021 | |
| dc.date.submitted | 2021-08-04 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/82323 | - |
| dc.description.abstract | 近幾年內，諸多研究指出長鏈非編碼 RNA 在癌症進程中扮演著致癌的角色。然而，長鏈非編碼 RNA對於影響腫瘤生長及轉移的詳細機制仍待釐清。在本篇研究，我們發現了一個與癌症相關的長鏈非編碼 RNA並取名為Smyca (Smad/Myc coactivator)，它的高度表現與多種癌症病人的不良預後呈正相關。從結構上觀察，Smyca的初級轉錄產物中，Smyca序列的5’ 端連接著一群微小RNA (miRNA)，而經過Drosha蛋白酶的切割後，則能使Smyca與這群微小RNA 分開。為了研究Smyca在癌症進程中具有哪些功能，我們首先利用能與Smyca序列互補的短髮夾RNA (shRNA)以有效降低Smyca的表現量，且不影響其上游端的微小RNA群表現。我們發現降低乳癌細胞中Smyca的表現量，會誘導其細胞型態會從間質型態轉換為上皮型態。隨後，我們實驗室使用RNA定序及生物資訊的分析，發現Smyca可能參與TGF-ꞵ訊號通路。而實驗也發現，過度表現Smyca的正常乳腺細胞會促進TGF-ꞵ訊號通路的中下游目標基因的表現量及啟動子的活性。然而，Smyca並不會影響TGF-ꞵ訊號通路過程中Smad蛋白的表現量及其磷酸化程度。在實驗室先前的研究成果中，發現Smyca本身的表現能被TGF-ꞵ所誘導。而後續的實驗證實，在過度表現Smyca的組別中會增長TGF-ꞵ訊號通路的強度與時間長度，因此表明Smyca會利用與TGF-ꞵ訊號通路形成的正回饋機制，加以調控TGF-ꞵ訊號通路。此外，我們實驗室也發現Smyca會連結到MYC蛋白並促進MYC下游基因表現。通常MYC需要與MAX結合形成一個穩定的異二聚體以誘導下游基因表現。因此，我們決定研究Smyca是否會透過促進MYC-MAX聚合物的形成，以影響MYC下游基因的表現。儘管如此，我們發現過度表現或降低表現Smyca都不會影響MYC與MAX的結合力，這暗示著Smyca可能透過其他機制以促進MYC下游基因的表現。總結，我們的實驗結果揭示了一個嶄新的長鏈非編碼 RNA調節TGF-ꞵ訊號通路的回饋機制，也發現此種長鏈非編碼 RNA還能參與提升MYC訊號通路。此外，我們的研究也闡釋了Smyca在癌症進程中的功能，及其詳細的分子調控機制。 | zh_TW |
| dc.description.provenance | Made available in DSpace on 2022-11-25T07:29:13Z (GMT). No. of bitstreams: 1 U0001-0208202115035400.pdf: 1775083 bytes, checksum: 194d12cc1f91812152ea54150b46fbb5 (MD5) Previous issue date: 2021 | en |
| dc.description.tableofcontents | "目 錄 口試委員會審定書………………………….……………………………………….i 謝辭………………………………………….………………………………..…….….ii 中文摘要………………………………………………………………………..….…iii 英文摘要………………………………………………………………………..….…iv I. Introduction……………………………………………………………………….1 1. EMT and its function in cancer progression……………………………………1 1.1 Overview of EMT…………………………………………..……………………..1 1.2 EMT in cancer progression………………………………….…………………....2 1.3 EMT and resistance to cancer therapies………………..……………………….4 2. Long noncoding RNA (LncRNA)…………………………………………………5 2.1 Overview of long noncoding RNA………………..…………………………5 2.2 Clinical significance of long noncoding RNA in cancer biology……………..6 2.3 Long noncoding RNA and EMT in cancer……………………………………7 3. TGF-ꞵ signaling pathway…………………………………………………………9 3.1 Overview of TGF-ꞵ signaling pathway……………………………………….9 3.2 The functions of TGF-ꞵ pathway in cancer…………………..…………...10 3.3 TGF-ꞵ signaling in EMT and EMT-related functions…………..…………...12 3.4 TGF‐β signaling and long non‐coding RNAs in cancer………..……………13 4. MYC……………………………………………………………………………15 4.1 Overview of MYC……………………………………………..………….15 4.2 MYC in tumor progression………………………………………………....17 4.3 Signaling interplay between MYC and TGF‐β…………………..………..18 4.4 Crosstalk between MYC and lncRNA in cancer………………..…………19 5. Smyca…………………………………………………………………………....21 5.1 The discovery of Smyca……………………………………………..……..21 5.2 Smyca in cancer……………………………………………………..……...21 II. Materials and methods…………………………………………………………..23 Cell culture………………………………………………………………………...23 Plasmids…………………………………………………………………………...23 Lentivirus transduction……………………………………………………………23 Quantification of miRNA-23a, miR-24-2 and miR-27a…………………………..24 RNA extraction and RT-qPCR…………………………………………………….25 Luciferase reporter assay and transfection………………………………………...26 Western blot and Smad2/3 phosphorylation assay………………………………...26 Co-immunoprecipitation (Co-IP) assay…………………………………………...28 Statistical analysis…………………………………………………………………28 III. Result…………………………………………………………………………...29 1. Smyca shRNAs downregulate Smyca expression without affecting the expression of miRNAs in the miR-23a~27a~24-2 cluster…………………………………29 2. Smyca induces MET in breast cancer cells………………………………......29 3. The modulation of Smyca influences TGF-ꞵ downstream genes………………30 4. Smyca promotes Smad-induced transactivaton without affecting Smad expression and phosphorylation………………………………………………………………………30 5. The positive feedback loop between Smyca and TGF-ꞵ signaling………………….31 6. Smyca does not affect Myc-Max binding…………………………………………….32 IV. Discussion……………………………………………………………………….33 V. Figures…………………………………………………………………………..38 Figure 1. Knockdown of Smyca doesn’t affect the expression levels of miR-23a~27a~24-2 cluster………………………………......................................……........38 Figure 2. Knockdown of Smyca induces MET…………………………………...…....39 Figure 3. Overexpression of Smyca promotes the expression of Smad target genes…..40 Figure 4. Knockdown of Smyca reduces the expression of Smad target gene c-Jun…..41 Figure 5. Overexpression of Smyca promotes the activity of Smad-responsive reporters………………………………………………………………………………..42 Figure 6. Knockdown of Smyca doesn’t affect Smad2/3 phosphorylation…….....…...43 Figure 7. Smyca enhances the amplitude and duration of TGF-ꞵ induced signaling.....44 Figure 8. Smyca doesn’t affect Myc-Max binding……………………………….……45 Figure 9. The feedback mechanism for Smyca in TGF-ꞵ pathway…………………....46 VI. Appendix……………………………………………………………….…..47 VII. References………………………………………………………………………48 " | |
| dc.language.iso | en | |
| dc.subject | MYC | zh_TW |
| dc.subject | 長鏈非編碼 RNA | zh_TW |
| dc.subject | Smyca | zh_TW |
| dc.subject | 癌症進程 | zh_TW |
| dc.subject | 間質上皮細胞轉化 | zh_TW |
| dc.subject | TGF-ꞵ | zh_TW |
| dc.subject | MET | en |
| dc.subject | MYC | en |
| dc.subject | Smyca | en |
| dc.subject | TGF-ꞵ pathway | en |
| dc.subject | lncRNA | en |
| dc.subject | cancer progression | en |
| dc.title | 長鏈非編碼 RNA Smyca藉由控制 TGF-ꞵ 訊號通路的回饋機制以促進腫瘤進程 | zh_TW |
| dc.title | Long non-coding RNA Smyca promotes tumor progression by controlling a feedback mechanism of TGF-ꞵ signaling | en |
| dc.date.schoolyear | 109-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 李育儒(Hsin-Tsai Liu),袁維謙(Chih-Yang Tseng) | |
| dc.subject.keyword | 長鏈非編碼 RNA,Smyca,癌症進程,間質上皮細胞轉化,TGF-ꞵ,MYC, | zh_TW |
| dc.subject.keyword | lncRNA,cancer progression,MET,Smyca,TGF-ꞵ pathway,MYC, | en |
| dc.relation.page | 63 | |
| dc.identifier.doi | 10.6342/NTU202101996 | |
| dc.rights.note | 同意授權(全球公開) | |
| dc.date.accepted | 2021-08-05 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 生化科學研究所 | zh_TW |
| dc.date.embargo-lift | 2024-08-12 | - |
| 顯示於系所單位： | 生化科學研究所 | |
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