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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
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dc.contributor.advisor | 郭彥彬(Yen-Ping Kuo) | |
dc.contributor.author | Chia-Ying Hsieh | en |
dc.contributor.author | 謝佳穎 | zh_TW |
dc.date.accessioned | 2021-06-15T00:59:35Z | - |
dc.date.available | 2008-09-11 | |
dc.date.copyright | 2008-09-11 | |
dc.date.issued | 2008 | |
dc.date.submitted | 2008-08-01 | |
dc.identifier.citation | Arredondo J, Chernyavsky AI, Grando SA (2006a). Nicotinic receptors mediate tumorigenic action of tobacco-derived nitrosamines on immortalized oral epithelial cells. Cancer Biol Ther 5: 511-7.
Arredondo J, Chernyavsky AI, Jolkovsky DL, Pinkerton KE, Grando SA (2006b). Receptor-mediated tobacco toxicity: cooperation of the Ras/Raf-1/MEK1/ERK and JAK-2/STAT-3 pathways downstream of alpha7 nicotinic receptor in oral keratinocytes. FASEB J 20: 2093-101. Arredondo J, Chernyavsky AI, Jolkovsky DL, Pinkerton KE, Grando SA (2007). Receptor-mediated tobacco toxicity: alterations of the NF-kappaB expression and activity downstream of alpha7 nicotinic receptor in oral keratinocytes. Life Sci 80: 2191-4. Arredondo J, Chernyavsky AI, Jolkovsky DL, Pinkerton KE, Grando SA (2008). Receptor-mediated tobacco toxicity: acceleration of sequential expression of alpha5 and alpha7 nicotinic receptor subunits in oral keratinocytes exposed to cigarette smoke. FASEB J 22: 1356-68. Arredondo J, Nguyen VT, Chernyavsky AI, Jolkovsky DL, Pinkerton KE, Grando SA (2001). A receptor-mediated mechanism of nicotine toxicity in oral keratinocytes. Lab Invest 81: 1653-68. Babic AM, Kireeva ML, Kolesnikova TV, Lau LF (1998). CYR61, a product of a growth factor-inducible immediate early gene, promotes angiogenesis and tumor growth. Proc Natl Acad Sci U S A 95: 6355-60. Banerjee AG, Gopalakrishnan VK, Vishwanatha JK (2007). Inhibition of nitric oxide-induced apoptosis by nicotine in oral epithelial cells. Mol Cell Biochem 305: 113-21. Brigstock DR (2002). Regulation of angiogenesis and endothelial cell function by connective tissue growth factor (CTGF) and cysteine-rich 61 (CYR61). Angiogenesis 5: 153-65. Brigstock DR (2003). The CCN family: a new stimulus package. J Endocrinol 178: 169-75. Chen CC, Mo FE, Lau LF (2001). The angiogenic factor Cyr61 activates a genetic program for wound healing in human skin fibroblasts. J Biol Chem 276: 47329-37. Chen Y, Du XY (2007). Functional properties and intracellular signaling of CCN1/Cyr61. J Cell Biochem 100: 1337-45. Chien W, Kumagai T, Miller CW, Desmond JC, Frank JM, Said JW et al (2004). Cyr61 suppresses growth of human endometrial cancer cells. J Biol Chem 279: 53087-96. Diniz-Freitas M, Garcia-Garcia A, Crespo-Abelleira A, Martins-Carneiro JL, Gandara-Rey JM (2004). Applications of exfoliative cytology in the diagnosis of oral cancer. Med Oral 9: 355-61. Gery S, Xie D, Yin D, Gabra H, Miller C, Wang H et al (2005). Ovarian carcinomas: CCN genes are aberrantly expressed and CCN1 promotes proliferation of these cells. Clin Cancer Res 11: 7243-54. Gerzanich V, Wang F, Kuryatov A, Lindstrom J (1998). alpha 5 Subunit alters desensitization, pharmacology, Ca++ permeability and Ca++ modulation of human neuronal alpha 3 nicotinic receptors. J Pharmacol Exp Ther 286: 311-20. Gotti C, Carbonnelle E, Moretti M, Zwart R, Clementi F (2000). Drugs selective for nicotinic receptor subtypes: a real possibility or a dream? Behav Brain Res 113: 183-92. Grandis JR, Drenning SD, Chakraborty A, Zhou MY, Zeng Q, Pitt AS et al (1998). Requirement of Stat3 but not Stat1 activation for epidermal growth factor receptor- mediated cell growth In vitro. J Clin Invest 102: 1385-92. Grandis JR, Drenning SD, Zeng Q, Watkins SC, Melhem MF, Endo S et al (2000). Constitutive activation of Stat3 signaling abrogates apoptosis in squamous cell carcinogenesis in vivo. Proc Natl Acad Sci U S A 97: 4227-32. Han JS, Macarak E, Rosenbloom J, Chung KC, Chaqour B (2003). Regulation of Cyr61/CCN1 gene expression through RhoA GTPase and p38MAPK signaling pathways. Eur J Biochem 270: 3408-21. Holley SL, Matthias C, Jahnke V, Fryer AA, Strange RC, Hoban PR (2005). Association of cyclin D1 polymorphism with increased susceptibility to oral squamous cell carcinoma. Oral Oncol 41: 156-60. Holloway SE, Beck AW, Girard L, Jaber MR, Barnett CC, Jr., Brekken RA et al (2005). Increased expression of Cyr61 (CCN1) identified in peritoneal metastases from human pancreatic cancer. J Am Coll Surg 200: 371-7. Huang M, Spitz MR, Gu J, Lee JJ, Lin J, Lippman SM et al (2006). Cyclin D1 gene polymorphism as a risk factor for oral premalignant lesions. Carcinogenesis 27: 2034-7. Jewett A, Wang MY, Teruel A, Poupak Z, Bostanian Z, Park NH (2003). Cytokine dependent inverse regulation of CD54 (ICAM1) and major histocompatibility complex class I antigens by nuclear factor kappaB in HEp2 tumor cell line: effect on the function of natural killer cells. Hum Immunol 64: 505-20. Jin Z, Gao F, Flagg T, Deng X (2004). Tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone promotes functional cooperation of Bcl2 and c-Myc through phosphorylation in regulating cell survival and proliferation. J Biol Chem 279: 40209-19. Kasten FH, Pineda LF, Schneider PE, Rawls HR, Foster TA (1989). Biocompatibility testing of an experimental fluoride releasing resin using human gingival epithelial cells in vitro. In Vitro Cell Dev Biol 25: 57-62. Kireeva ML, Mo FE, Yang GP, Lau LF (1996). Cyr61, a product of a growth factor-inducible immediate-early gene, promotes cell proliferation, migration, and adhesion. Mol Cell Biol 16: 1326-34. Ko YC, Huang YL, Lee CH, Chen MJ, Lin LM, Tsai CC (1995). Betel quid chewing, cigarette smoking and alcohol consumption related to oral cancer in Taiwan. J Oral Pathol Med 24: 450-3. Lee HJ, Guo HY, Lee SK, Jeon BH, Jun CD, Park MH et al (2005). Effects of nicotine on proliferation, cell cycle, and differentiation in immortalized and malignant oral keratinocytes. J Oral Pathol Med 34: 436-43. Leeman RJ, Lui VW, Grandis JR (2006). STAT3 as a therapeutic target in head and neck cancer. Expert Opin Biol Ther 6: 231-41. Li Y, St John MA, Zhou X, Kim Y, Sinha U, Jordan RC et al (2004). Salivary transcriptome diagnostics for oral cancer detection. Clin Cancer Res 10: 8442-50. Lin MT, Chang CC, Chen ST, Chang HL, Su JL, Chau YP et al (2004). Cyr61 expression confers resistance to apoptosis in breast cancer MCF-7 cells by a mechanism of NF-kappaB-dependent XIAP up-regulation. J Biol Chem 279: 24015-23. Lin MT, Zuon CY, Chang CC, Chen ST, Chen CP, Lin BR et al (2005). Cyr61 induces gastric cancer cell motility/invasion via activation of the integrin/nuclear factor-kappaB/cyclooxygenase-2 signaling pathway. Clin Cancer Res 11: 5809-20. Lindstrom J, Anand R, Peng X, Gerzanich V, Wang F, Li Y (1995). Neuronal nicotinic receptor subtypes. Ann N Y Acad Sci 757: 100-16. Mayr B, Montminy M (2001). Transcriptional regulation by the phosphorylation-dependent factor CREB. Nat Rev Mol Cell Biol 2: 599-609. Menendez JA, Mehmi I, Griggs DW, Lupu R (2003). The angiogenic factor CYR61 in breast cancer: molecular pathology and therapeutic perspectives. Endocr Relat Cancer 10: 141-52. Mo FE, Muntean AG, Chen CC, Stolz DB, Watkins SC, Lau LF (2002). CYR61 (CCN1) is essential for placental development and vascular integrity. Mol Cell Biol 22: 8709-20. Nguyen N, Kuliopulos A, Graham RA, Covic L (2006). Tumor-derived Cyr61(CCN1) promotes stromal matrix metalloproteinase-1 production and protease-activated receptor 1-dependent migration of breast cancer cells. Cancer Res 66: 2658-65. O'Brien TP, Yang GP, Sanders L, Lau LF (1990). Expression of cyr61, a growth factor-inducible immediate-early gene. Mol Cell Biol 10: 3569-77. Robertson C (2006). What are the roles of surgery, radiation therapy and chemotherapy in the treatment of oral cancer? J Can Dent Assoc 72: 529-30. Sato M, Sato T, Izumo T, Amagasa T (1999). Genetic polymorphism of drug-metabolizing enzymes and susceptibility to oral cancer. Carcinogenesis 20: 1927-31. Schuller HM (2007). Nitrosamines as nicotinic receptor ligands. Life Sci 80: 2274-80. Schuller HM, McGavin MD, Orloff M, Riechert A, Porter B (1995). Simultaneous exposure to nicotine and hyperoxia causes tumors in hamsters. Lab Invest 73: 448-56. Sreelekha TT, Ramadas K, Pandey M, Thomas G, Nalinakumari KR, Pillai MR (2001). Genetic polymorphism of CYP1A1, GSTM1 and GSTT1 genes in Indian oral cancer. Oral Oncol 37: 593-8. Sturgis EM, Dahlstrom KR, Guan Y, Eicher SA, Strom SS, Spitz MR et al (2001). Alcohol dehydrogenase 3 genotype is not associated with risk of squamous cell carcinoma of the oral cavity and pharynx. Cancer Epidemiol Biomarkers Prev 10: 273-5. Tsai MS, Bogart DF, Li P, Mehmi I, Lupu R (2002). Expression and regulation of Cyr61 in human breast cancer cell lines. Oncogene 21: 964-73. Tsai MS, Hornby AE, Lakins J, Lupu R (2000). Expression and function of CYR61, an angiogenic factor, in breast cancer cell lines and tumor biopsies. Cancer Res 60: 5603-7. Tsantoulis PK, Kastrinakis NG, Tourvas AD, Laskaris G, Gorgoulis VG (2007). Advances in the biology of oral cancer. Oral Oncol 43: 523-34. Waggoner SE, Wang X (1994). Effect of nicotine on proliferation of normal, malignant, and human papillomavirus-transformed human cervical cells. Gynecol Oncol 55: 91-5. Wang D, Ritchie JM, Smith EM, Zhang Z, Turek LP, Haugen TH (2005). Alcohol dehydrogenase 3 and risk of squamous cell carcinomas of the head and neck. Cancer Epidemiol Biomarkers Prev 14: 626-32. Wang T, Niu G, Kortylewski M, Burdelya L, Shain K, Zhang S et al (2004). Regulation of the innate and adaptive immune responses by Stat-3 signaling in tumor cells. Nat Med 10: 48-54. Westra WH, Califano J (2004). Toward early oral cancer detection using gene expression profiling of saliva: a thoroughfare or dead end? Clin Cancer Res 10: 8130-1. Wright SC, Zhong J, Zheng H, Larrick JW (1993). Nicotine inhibition of apoptosis suggests a role in tumor promotion. FASEB J 7: 1045-51. Xie D, Yin D, Tong X, O'Kelly J, Mori A, Miller C et al (2004). Cyr61 is overexpressed in gliomas and involved in integrin-linked kinase-mediated Akt and beta-catenin-TCF/Lef signaling pathways. Cancer Res 64: 1987-96. Xu J, Huang H, Pan C, Zhang B, Liu X, Zhang L (2007). Nicotine inhibits apoptosis induced by cisplatin in human oral cancer cells. Int J Oral Maxillofac Surg 36: 739-44. Yang GP, Lau LF (1991). Cyr61, product of a growth factor-inducible immediate early gene, is associated with the extracellular matrix and the cell surface. Cell Growth Differ 2: 351-7. Ye YN, Liu ES, Shin VY, Wu WK, Cho CH (2004). The modulating role of nuclear factor-kappaB in the action of alpha7-nicotinic acetylcholine receptor and cross-talk between 5-lipoxygenase and cyclooxygenase-2 in colon cancer growth induced by 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone. J Pharmacol Exp Ther 311: 123-30. Zheng Y, Shen H, Sturgis EM, Wang LE, Eicher SA, Strom SS et al (2001). Cyclin D1 polymorphism and risk for squamous cell carcinoma of the head and neck: a case-control study. Carcinogenesis 22: 1195-9. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/42316 | - |
dc.description.abstract | 根據衛生署公佈之國人「十大死亡原因」,癌症已蟬聯第一位達二十一年之久;其中口腔癌的發生率及死亡率位居國內男性十大癌症之第四位及第五位,且又以鱗狀上皮細胞癌(squamous cell carcinoma, SCC)最為常見。許多研究已證實菸草內之致癌物質為促使口腔癌發生的重要因素之一,而尼古丁(nicotine)為菸草中最主要的成分。尼古丁可改變細胞的功能,如生長、附著,及matrix protein之合成等。Cyr61為CCN family中的成員,參與調控細胞之附著、移動、增生、分化、凋亡及血管新生等,在許多癌症中被指出與癌症生成有關。本實驗室先前的研究中發現,口腔癌病人癌化組織中有較正常組織高的Cyr61表現。轉殖過量表現Cyr61之細胞株至SCID小鼠體內則可增加腫瘤之體積及增進血管新生之情形,顯示Cyr61和口腔癌之間有著密不可分的關係。本研究主旨即為了解尼古丁在口腔上皮細胞中是否會活化Cyr61的表現,並探討其訊息傳導路徑。我們發現10μM 尼古丁可誘導正常人類口腔上皮細胞株S-G及口腔癌細胞株Ca-922與KB之Cyr61蛋白表現。KB之Cyr61蛋白和mRNA在尼古丁刺激0.5小時後開始上升,分別於2小時及0.5小時達到高峰之後開始下降,8小時及2小時後降回正常值。當加入α3、α7與α9 nicotinic acetylcholine receptor (nAchR)之抑制劑d-tubocurarine及α7 nAchR之抑制劑MG 624時可反轉Cyr61被活化之情形,但α3 nAchR抑制劑macamylamine和α9抑制劑strychnine則無此效果,且單獨以α7 nAchR之促進劑choline處理KB亦使Cyr61表現量提升,顯示尼古丁係經含有α7但不含α3與α9 subtype之nAchR誘導Cyr61表現。muscarinic acetylcholine receptor (mAchR) M2及M3 mAchR抑制劑4-DAMP與gallamine並無此影響,顯示尼古丁非經由mAchR刺激Cyr61表現。以 p38 MAPK之抑制劑SB203580前處理可阻斷尼古丁所誘導之Cyr61蛋白表現,顯示此活化路徑極可能經由p38 MAPK達成;但MSK1、PKA與Rho A GTPase抑制劑無此影響,顯示尼古丁並非經由這些路徑誘導Cyr61蛋白表現。本論文首次指出尼古丁可經由p38 MAPK訊息傳遞路徑誘導Cyr61蛋白之表現。冀望未來可藉由抑制此訊息傳遞路徑之成員來達到抑制抽菸導致的口腔癌之目的。 | zh_TW |
dc.description.abstract | According to the top 10 causes of death in Taiwan published by the department of health, cancer has been the top 1 for 21 years. The occurrence rate and mortality rate of oral cancer is the top four and top five of the ten most common cancers of Taiwanese male, respectively. Among oral caner, squamous cell carcinoma (SCC) is the most common one. Many researches had proved that the carcinogen in tobacco is one of the most important causes of oral cancer, and nicotine is one of the main components of tobacco. Nicotine can alter the cell functions, such like the growth and adhesion of the cells, and the production of matrix protein. Cyr61 is a member of the CCN family, which involves the regulation of cell adhesion, migration, proliferation, differentiation, apoptosis and angiogenesis, and was reported to be related to the occurrence of cancer. Previous study of our laboratory found that there was much higher expression of Cyr61 in the cancerous tissue of oral cancer patients than that of normal tissue; Cyr61 overexpressing transgenic SCID mice had larger tumor and improvement of angiogenesis. These data indicated that Cyr61 is closely related to oral cancer. The main purpose of this research is to find out whether nicotine can induce the expression of Cyr61 in the oral epithelial cells and to investigate the signaling pathway. We found that 10μM nicotine could induce the protein expression of the normal epithelial cell line S-G cells and the cancerous cell lines Ca9-22 and KB. The expression of protein and mRNA of Cyr61 in KB was elevated after treatment of 0.5 hour, and reached a high after 2 and 0.5 hours, and returned to the origin after 8 and 2 hours, respectively. Pre-treatment of KB cells with the inhibitor of α3、α7 and α9 nicotinic acetylcholine receptor (nAchR) d-tubocurarine and the inhibitor of α7 nAchR MG 624 but not the inhibitor of α3 nAchR macamylamine and that of α9 nAchR strychnine reversed the activation of Cyr61 expression; treatment of α7 nAchR agonist choline alone also stimulated Cyr61 expression, indicated that nicotine induced Cyr61 expression through α7-containing but not α3- and α9- containing nAchR. The inhibitor of cholinergic receptor atropine but not the inhibitor of M2 and M3 muscarinic acetylcholine receptor (mAchR) 4-DAMP and gallamine could suppress Cyr61 expression, proved that the activation was not through the mAchR. The expression of Cyr61 could be blocked by pre-treatment of p38 MAPK inhibitor SB203580 showed that p38 probably participated in the activation pathway, and other specific inhibitors had ruled out the possibility of involvement of MSK1, PKA and the Rho A GTPase family. This article showed that nicotine could induce the expression of Cyr61 through p38 MAPK pathway for the first time, and the signaling pathway can be the target of treating the oral cancer caused by smoking. | en |
dc.description.provenance | Made available in DSpace on 2021-06-15T00:59:35Z (GMT). No. of bitstreams: 1 ntu-97-R95450017-1.pdf: 1739348 bytes, checksum: 5bd7884d4a5251928c72e0f6c45a063e (MD5) Previous issue date: 2008 | en |
dc.description.tableofcontents | 中文摘要 1
Abstract 2 導論(Introduction) 4 第一節 口腔癌(oral cancer)4 第二節 尼古丁(nicotine)7 第三節 Cyr61 10 第四節 研究動機 13 材料與方法 (Materials and Methods)14 細胞培養(cell culture)14 藥物處理(drug treatment)14 蛋白質萃取(protein extraction)15 西方墨點法(western blot)15 RNA萃取(RNA extraction)16 反轉錄(reverse transcription)17 即時聚合酶連鎖反應 (real-time PCR)17 結果(Results)19 尼古丁可誘導口腔上皮細胞中Cyr61蛋白的表現19 尼古丁可刺激KB細胞中Cyr61之mRNA表現量上升19 尼古丁經由含有α7但不含α3及 α9 subtype之nAchR誘導Cyr61表現19 尼古丁經由p38訊息傳導路徑誘導Cyr61表現 20 尼古丁誘導Cyr61表現並非經由MSK1及 PKA 20 Rho A GTPase family不涉及尼古丁誘導Cyr61表現21 討論(Discussion)22 圖與表(Figures and Tables)25 參考文獻(References)43 | |
dc.language.iso | zh-TW | |
dc.title | 尼古丁誘導口腔上皮細胞中Cyr61之表現及其機轉 | zh_TW |
dc.title | Nicotine induced the expression of Cyr61 in oral epithelial cells | en |
dc.type | Thesis | |
dc.date.schoolyear | 96-2 | |
dc.description.degree | 碩士 | |
dc.contributor.coadvisor | 林思洸(Sze-Kwan Lin) | |
dc.contributor.oralexamcommittee | 蕭宏昇(Hong-Shen Hsiao) | |
dc.subject.keyword | 口腔癌,口腔上皮細胞,尼古丁, | zh_TW |
dc.subject.keyword | oral cancer,oral epithelial cells,nicotine, | en |
dc.relation.page | 47 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2008-08-01 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 口腔生物科學研究所 | zh_TW |
顯示於系所單位: | 口腔生物科學研究所 |
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