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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 賈景山(Jean-San Chia) | |
| dc.contributor.author | I-Ling Yu | en |
| dc.contributor.author | 余翊菱 | zh_TW |
| dc.date.accessioned | 2021-06-17T04:26:42Z | - |
| dc.date.available | 2018-09-04 | |
| dc.date.copyright | 2018-09-04 | |
| dc.date.issued | 2018 | |
| dc.date.submitted | 2018-08-14 | |
| dc.identifier.citation | Cahalan, M. D. (2009). 'STIMulating store-operated Ca(2+) entry.' Nat Cell Biol 11(6): 669-677.
Chen, Y. F., W. T. Chiu, Y. T. Chen, P. Y. Lin, H. J. Huang, C. Y. Chou, H. C. Chang, M. J. Tang and M. R. Shen (2011). 'Calcium store sensor stromal-interaction molecule 1-dependent signaling plays an important role in cervical cancer growth, migration, and angiogenesis.' Proc Natl Acad Sci U S A 108(37): 15225-15230. Lewis, R. S. (2001). 'Calcium signaling mechanisms in T lymphocytes.' Annu Rev Immunol 19: 497-521. Li, Y., B. Guo, Q. Xie, D. Ye, D. Zhang, Y. Zhu, H. Chen and B. Zhu (2015). 'STIM1 Mediates Hypoxia-Driven Hepatocarcinogenesis via Interaction with HIF-1.' Cell Rep 12(3): 388-395. Liu, X., B. Gong, L. B. de Souza, H. L. Ong, K. P. Subedi, K. T. Cheng, W. Swaim, C. Zheng, Y. Mori and I. S. Ambudkar (2017). 'Radiation inhibits salivary gland function by promoting STIM1 cleavage by caspase-3 and loss of SOCE through a TRPM2-dependent pathway.' Sci Signal 10(482). Pathak, T., T. Agrawal, S. Richhariya, S. Sadaf and G. Hasan (2015). 'Store-Operated Calcium Entry through Orai Is Required for Transcriptional Maturation of the Flight Circuit in Drosophila.' J Neurosci 35(40): 13784-13799. Prakriya, M., S. Feske, Y. Gwack, S. Srikanth, A. Rao and P. G. Hogan (2006). 'Orai1 is an essential pore subunit of the CRAC channel.' Nature 443(7108): 230-233. Prakriya, M. and R. S. Lewis (2003). 'CRAC channels: activation, permeation, and the search for a molecular identity.' Cell Calcium 33(5-6): 311-321. Schmidt, S., G. Liu, G. Liu, W. Yang, S. Honisch, S. Pantelakos, C. Stournaras, A. Honig and F. Lang (2014). 'Enhanced Orai1 and STIM1 expression as well as store operated Ca2+ entry in therapy resistant ovary carcinoma cells.' Oncotarget 5(13): 4799-4810. Shaw, P. J. and S. Feske (2012). 'Physiological and pathophysiological functions of SOCE in the immune system.' Front Biosci (Elite Ed) 4: 2253-2268. Stewart, T. A., K. T. Yapa and G. R. Monteith (2015). 'Altered calcium signaling in cancer cells.' Biochim Biophys Acta 1848(10 Pt B): 2502-2511. Wang, J. Y., J. Sun, M. Y. Huang, Y. S. Wang, M. F. Hou, Y. Sun, H. He, N. Krishna, S. J. Chiu, S. Lin, S. Yang and W. C. Chang (2015). 'STIM1 overexpression promotes colorectal cancer progression, cell motility and COX-2 expression.' Oncogene 34(33): 4358-4367. Xu, Y., S. Zhang, H. Niu, Y. Ye, F. Hu, S. Chen, X. Li, X. Luo, S. Jiang, Y. Liu, Y. Chen, J. Li, R. Xiang and N. Li (2015). 'STIM1 accelerates cell senescence in a remodeled microenvironment but enhances the epithelial-to-mesenchymal transition in prostate cancer.' Sci Rep 5: 11754. Yan, X., J. Xing, C. Lorin-Nebel, A. Y. Estevez, K. Nehrke, T. Lamitina and K. Strange (2006). 'Function of a STIM1 homologue in C. elegans: evidence that store-operated Ca2+ entry is not essential for oscillatory Ca2+ signaling and ER Ca2+ homeostasis.' J Gen Physiol 128(4): 443-459. Yang, N., Y. Tang, F. Wang, H. Zhang, D. Xu, Y. Shen, S. Sun and G. Yang (2013). 'Blockade of store-operated Ca(2+) entry inhibits hepatocarcinoma cell migration and invasion by regulating focal adhesion turnover.' Cancer Lett 330(2): 163-169. Zhang, Z., X. Liu, B. Feng, N. Liu, Q. Wu, Y. Han, Y. Nie, K. Wu, Y. Shi and D. Fan (2015). 'STIM1, a direct target of microRNA-185, promotes tumor metastasis and is associated with poor prognosis in colorectal cancer.' Oncogene 34(37): 4808-4820. https://org.vghks.gov.tw https://www.cancer.org | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/70368 | - |
| dc.description.abstract | To escape from the primary tumor site, metastatic cancer cells acquire the abilities to invade and migrate partially through Ca2+ signaling-regulated cytoskeleton rearrangement and focal adhesion dynamics. To maintain physiological homeostasis, intracellular Ca2+ pool is tightly controlled via store-operated calcium entry (SOCE), which includes the activation of stromal interaction molecules (STIM) upon Ca2+ depletion within the endoplasmic reticulum, followed by the activation of Ca2+-selective channel ORAI on the plasma membrane to replenish Ca2+ from extracellular space. Several studies have revealed aberrant levels of STIM1 in human cancers such as breast cancer, renal cell carcinoma and colorectal cancer, but whether STIM1 aberrancy affects SOCE activities or other signaling pathways to induce cancer cell migration or invasion were still unclear. Our preliminary results indicated that expression levels of STIM1 were associated with the progression of oral cancer. Oral cancer in the domestic prevalence rate is very high, and in the domestic top ten cancers, may have a considerable relationship with the diet culture, of which oral squamous cell carcinoma (OSCC) is one of the most common oral cancer, and prone to cervical lymph node metastasis. At present, the treatment of oral cancer is mainly surgical resection, combined with radiotherapy, but often a certain proportion of patients appear treatment resistance. Therefore, this study is intended to investigate the hypothesis of lymph node metastasis and radiotherapy in oral cancer cells regulated by STIM1. Reduction of SOCE activities targeting STIM1 by shRNA in oral squamous cell carcinoma (OSCC), or over-expressing STIM1 to see whether it affects the proliferation and invasive ability of cancer cells, Immunohistochemical (IHC) staining was used to see the difference of STIM1 in situ carcinoma and metastatic site. We also used the Xenograft mouse models to observe the role of STIM1 in lymph node metastasis and how to influence radiation therapy. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-17T04:26:42Z (GMT). No. of bitstreams: 1 ntu-107-R05450007-1.pdf: 3869169 bytes, checksum: 5b8ed3133afed06f486ae86a748e706a (MD5) Previous issue date: 2018 | en |
| dc.description.tableofcontents | 致謝 1
中文摘要 2 英文摘要 3 目錄 5 章節1 前言 7 1.1 口腔癌 7 1.2 鈣池調控離子通道(SOCE) 8 1.3 鈣池調控鈣離子通道(SOCE)控制各種生理及病理的過程 8 1.4 STIM1參與在不同的癌症當中 9 1.5 放射治療 9 章節2 假說及目的 11 章節3 材料與方法 12 3.1 細胞株及細胞培養 12 3.2 西方點墨法 13 3.3 慢病毒製作的穩定靜默基因(shRNA) 13 3.4 慢病毒製作的穩定過量表達基因 14 3.5 免疫組織化學染色法 14 3.6 細胞移行及侵入實驗法 15 3.7 動物實驗 15 章節4 結果 17 4.1 在口腔鱗狀細胞癌細胞株中STIM1的表現量及爬行的速度 17 4.2 打入SAS-Luc-shSTIM1細胞的原位異種移植模型來看轉移的現象 17 4.3 原發性腫瘤與轉移性腫瘤之間STIM1表現量的差異 18 4.4 探討STIM1是否參與口腔癌細胞的侵襲及增加放射的耐受性 18 4.5 用動物實驗來驗證離體實驗的結果 19 章節5 討論 21 章節6 參考文獻 23 章節7 表 25 表1.慢病毒製作的穩定靜默基因控制組之序列 25 表2. 慢病毒製作的穩定靜默人類STIM1基因之序列 25 表3. 慢病毒製作的穩定過量表達基因 25 章節8 圖 26 圖 1.比較STIM1的表現量在異體移植的老鼠中原位腫瘤與轉移腫瘤的差異 27 圖2.測量慢病毒製備成的SAS-Luc,SAS-Luc-STIM1細胞株及SAS-shRNA細胞株的感染效率 29 圖 3.將SAS細胞株做shSTIM1及STIM1過量表達的處理後會使細胞移行及侵襲能力增加 31 圖 4.觀察原位接種口腔癌細胞(SAS,SAS-Luc,SAS-Luc-STIM1)的老鼠，其腫瘤生長及轉移的情況 33 圖 5.觀察STIM1對異位接種口腔癌細胞的老鼠其腫瘤生長及放射反應的影響 34 章節9 附件 36 附件1.STIM1的表現量與口腔癌臨床結果及癌症轉移的相關性 36 附件 2.在口腔鱗狀細胞癌細胞株中比較STIM1的表現量及細胞移行 37 附件3.觀察打入SAS-shLuc,SAS-shSTIM1細胞株之老鼠腫瘤的轉移情況 39 附件 4.打入SAS-shLuc,SAS-shSTIM1細胞株之老鼠的轉移數量及腫瘤大小 40 | |
| dc.language.iso | zh-TW | |
| dc.subject | 放射治療 | zh_TW |
| dc.subject | 口腔鱗狀細胞癌細胞 | zh_TW |
| dc.subject | 基質交互分子 | zh_TW |
| dc.subject | 侵襲 | zh_TW |
| dc.subject | STIM1 | en |
| dc.subject | OSCC | en |
| dc.subject | invasion | en |
| dc.subject | radiation | en |
| dc.title | STIM1在口腔癌細胞的侵襲及放射反應中所扮演的角色 | zh_TW |
| dc.title | The Role of STIM1 in Radioresponse and Invasion of Oral Cancer Cells | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 106-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 蔡丰喬(Feng-Chiao Tsai),張玉芳(Yu-Fang Chang) | |
| dc.subject.keyword | 基質交互分子,口腔鱗狀細胞癌細胞,放射治療,侵襲, | zh_TW |
| dc.subject.keyword | STIM1,OSCC,radiation,invasion, | en |
| dc.relation.page | 40 | |
| dc.identifier.doi | 10.6342/NTU201803227 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2018-08-14 | |
| 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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