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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 俞松良(Sung-Liang Yu) | |
dc.contributor.author | Chun-Chieh Chen | en |
dc.contributor.author | 陳俊杰 | zh_TW |
dc.date.accessioned | 2021-06-08T00:25:21Z | - |
dc.date.copyright | 2013-09-24 | |
dc.date.issued | 2013 | |
dc.date.submitted | 2013-07-15 | |
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/17613 | - |
dc.description.abstract | 癌症目前是全世界最受矚目的公眾健康議題,在美國每四人死亡就有一人是因為罹癌。無論在台灣或全世界,肺癌是占癌症死亡的首位,而大腸直腸癌的發生率及死亡率在台灣與已開發國家皆不斷逐年上升。縱使近年來癌症偵測有顯著的進步,但多數的癌症仍於晚期方被診斷出,同時治療的結果尚未臻滿意。癌症轉移乃因癌細胞擴散及遠端器官腫瘤生長,此乃導致癌症致死最主要的原因。因此,為了降低腫瘤復發及轉移所造成的癌症死亡,深入地研究及探討癌轉移機制實為刻不容緩之事。近年伴隨著轉譯醫學的蓬勃發展,癌症個人化醫療更備受重視。對於癌症分子標靶治療而言,發展新的癌症生物標記、標靶基因和治療藥物對病人亦是極為重要。然而,抗藥性的產生為目前癌症分子標靶治療所遇到的最大困境,尤其是肺癌。本實驗室之前的研究發現,不論在活體內或體外,中草藥薑黃的主要成分薑黃素(curcumin)對艾瑞莎(Iressa®, Gefitinib)具抗藥性的肺癌細胞株具有明顯的抑制生長能力並且會增強艾瑞莎對抗藥性細胞株的抑癌活性。本研究主要利用兩種不同觀點,分別從基因及藥物治療層面各別探討抑制兩種具代表性的癌症(肺癌及大腸直腸癌)腫瘤轉移之機制。首先,我們利用array CGH以及expression microarrays兩種不同實驗平台來分析兩種不同侵犯程度的肺癌細胞株,發現在染色體位置4p13的區域有一新穎且和腫瘤侵犯相關的基因,名為shisa3。我們發現在高度侵襲的肺癌細胞株中,shisa3基因的DNA拷貝數及mRNA和蛋白質的表現量皆非常低。本研究更指出此基因不但可以在活體外抑制肺腺癌細胞株的侵犯能力、移動能力以及生長能力,還可在活體內抑制腫瘤的生長及轉移。此外,shisa3基因會透過WNT/β-catenin傳導路徑來調控EMT現象,並從非小細胞肺癌的病人身上可發現當shisa3基因低度表現時與癌轉移有高度相關性,且存活率較差。再者,我們利用薑黃素來處理大腸直腸癌細胞株探討其影響癌轉移之機制。結果指出薑黃素不但在活體外可抑制大腸直腸癌細胞株的移動能力、侵犯能力以及生長能力,還可在活體內抑制腫瘤生長及肝轉移。總結以上,我們發現薑黃素會透過抑制Sp1, FAK, CD24以及促進E-cadherin的表現量,來抑制大腸直腸癌細胞株的癌轉移能力。 | zh_TW |
dc.description.abstract | Cancer is a most important and popular issue of public health globally and which causes about 25% death in the United States. Lung cancer is the leading cause of cancer death in Taiwan and worldwide. The incidence and mortality of colorectal cancer (CRC) is increasing in Taiwan and many developed countries. Although the development of cancer detection is greatly progressed recently, the majority of cancers are diagnosed at late stages and the therapeutic outcome is still not satisfied. Metastasis causes the major death of all cancers due to dissemination and outgrowth of tumors at distant organs. To reduce cancer mortality caused by recurrence and metastasis the understanding of mechanisms involved in cancer progression in depth is urgently needed. Recent years, personalized medicine has become the most important issue globally which is due to the advanced development of translational medicine. Hence, how to identify potential genes as cancer biomarkers and druggable targets and to develop therapeutic drugs for molecular-targeted therapy are helpful to cancer patients. However, the challenge confronted by targeted cancer therapies is the development of drug resistance. Our previous report indicated that a component of Chinese herbal medicine, curcumin, could inhibit cell proliferation and improve the efficiency of gefitinib in the gefitinib-resistant lung cells in vitro and in vivo. Here, we investigate the underlying anti-metastasis mechanism with different views from genetic and pharmacotherapeutic aspects in two representative cancers, lung cancer and CRC. First, we identify a novel invasion-associated gene, shisa3, which is located on chromosome 4p13 by using array CGH (comparative genomic hybridization) and expression microarrays with two lung adenocarcinoma cell lines among varied invasive ability. The gene copy number, mRNA and protein expression of shisa3 is decreased in highly invasive cells significantly. Here, we report that shisa3 is a potential tumor suppressor, which inhibits the cell invasion, migration, proliferation and anchorage-independent growth of lung adenocarcinoma cells in vitro and it also inhibits metastasis and tumorigenesis in vivo. We not only explore that shisa3 may reverse the EMT through WNT/β-catenin signaling pathway but also find that low shisa3 expression are associated with lung metastasis and poor survival in non-small-cell lung cancer (NSCLC) patients. Moreover, we explore the underlying molecular mechanisms of curcumin on metastasis of CRC cells in vitro and in vivo. The results indicate that curcumin not only significantly inhibits cell migration, invasion and colony formation in vitro, but also reduces tumor growth and liver metastasis in vivo. Together all, we suggest that curcumin executes its anti-metastasis function through down-regulation of Sp1, FAK, CD24, and by promoting E-cadherin expression in CRC cells. | en |
dc.description.provenance | Made available in DSpace on 2021-06-08T00:25:21Z (GMT). No. of bitstreams: 1 ntu-102-D96424001-1.pdf: 6152932 bytes, checksum: 7b0cb3c5e815c2259516cbdbbd5bdf14 (MD5) Previous issue date: 2013 | en |
dc.description.tableofcontents | Acknowledgement i
中文摘要 iii Abstract v Contents vii List of Figures x List of Tables xii Chapter I: Shisa3, a Novel Tumor Suppressor, Inhibits Metastasis through WNT/β-catenin Signaling Pathway in Lung Cancer 1 A. Abstract 2 B. Introduction 3 1. Lung cancer 5 2. Histological classification of lung cancer 7 3. Tumor migration, invasion and metastasis 10 4. Epithelial-mesenchymal transition (EMT) 12 5. WNT/β-catenin signaling pathway 14 6. Multi-faceted roles of β‑catenin 18 7. Shisa families 20 8. Genetic alteration in lung cancer 21 C. Materials and Methods 28 1. Sample collection and immunohistochemistry 28 2. Cell culture 29 3. Transfection 29 4. Quantitative real-time PCR 30 5. Cell lysate preparation, immunoprecipitation and immunoblotting 31 6. Antibodies 32 7. Matrigel invasion assay 32 8. Cell migration assay 33 9. In vivo tumorigenesis and metastasis 33 10. Luciferase assay 35 11. Pulse–chase analysis 35 12. Statistical analysis 36 13. Array CGH 36 D. Results 38 1. Shisa3 is a novel tumor suppressor gene in lung cancer 38 2. N-terminal abolished shisa3 disrupts its tumor suppressor function 41 3. Shisa3 inhibits angiogenesis in lung adenocarcinoma 42 4. Shisa3 inhibits tumorigenesis and metastasis in vivo 43 5. Shisa3-induced β-catenin degradation is 26S proteosome-dependent 45 6. Shisa3 reverses EMT by decreasing β-catenin 47 7. Shisa3 accelerates β-catenin degradation through decrease of WNT receptors availability 48 8. Down-regulation of shisa3 correlates with poor survival in early stage of non-small-cell lung cancer (NSCLC) 50 E. Discussion 53 Chapter II: Curcumin Suppresses Metastasis via Sp-1, FAK Inhibition and E-cadherin Upregulation in Colorectal Cancer (CRC) 59 A. Abstract 60 B. Introduction 61 1. Population of CRC 66 2. Staging of CRC 67 3. Management and prognosis of CRC 69 4. Metastasis and clinical limit of CRC 70 5. Pathogenesis of CRC 70 6. Chemical properties and traditional uses of curcumin 71 7. Anti-cancer therapies of curcumin 72 8. Cancer metastasis and curcumin 74 9. Effect of curcumin on CRC 74 C. Materials and Methods 76 1. Cell lines and cell culture 76 2. Cell viability assay 76 3. Wound healing assay 76 4. Matrigel invasion assay 77 5. Transwell migration assay 77 6. Anchorage independent colony formation assay 78 7. In vivo mouse model 78 8. RNA extraction 79 9. Microarray analysis 79 10. Quantitative real-time PCR 80 11. Western blot analysis 81 12. Cell adhesion assay 82 13. Sp-1 luciferase assay 83 D. Results 84 1. Curcumin inhibits proliferation, migration, invasion and colony formation of CRC cell lines. 84 2. Curcumin inhibits tumor growth and liver metastasis in vivo 86 3. Microarray analysis of gene expression of HCT-116 cells after treatment with curcumin 86 4. Curcumin inhibits CD24 expression in HCT-116 cells 87 5. Curcumin suppresses Sp-1 transcriptional activity and its downstream gene expression 88 6. Effect of curcumin on FAK-regulated cytoskeleton remodeling and cell adhesion pathways 89 7. The potential inhibitory effect of curcumin on epithelial-mesenchymal transition 90 E. Discussion 91 1. Potential role of FAK signaling in the anti-metastasis effect of curcumin 92 2. Curcumin down-regulates CD24 in CRC 94 3. Curcumin enhances E-cadherin expression in CRC cells 95 4. Potential role of EMT in anti-metastasis effect of curcumin 96 5. Conclusion 98 Figures 99 Tables 156 References 162 Appendices 188 | |
dc.language.iso | en | |
dc.title | 從基因及藥物治療觀點探討癌症轉移 | zh_TW |
dc.title | Investigation of Cancer Metastasis from Genetic and Pharmacotherapeutic Aspects | en |
dc.type | Thesis | |
dc.date.schoolyear | 101-2 | |
dc.description.degree | 博士 | |
dc.contributor.oralexamcommittee | 陳健尉(Jeremy J.W. Chen),楊雅倩(Ya-Chien Yang),顏伯勳(Bo-Shiun Yan),陳惠文(Huei-Wen Chen) | |
dc.subject.keyword | 肺癌,大腸直腸癌,癌轉移,個人化醫療,轉譯醫學,薑黃素,shisa3, | zh_TW |
dc.subject.keyword | lung cancer,colorectal cancer (CRC),metastasis,personalized medicine,translational medicine,Curcumin,shisa3, | en |
dc.relation.page | 188 | |
dc.rights.note | 未授權 | |
dc.date.accepted | 2013-07-15 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 醫學檢驗暨生物技術學研究所 | zh_TW |
顯示於系所單位: | 醫學檢驗暨生物技術學系 |
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