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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 賈景山 | |
dc.contributor.author | Chih-Ying Lin | en |
dc.contributor.author | 林芷穎 | zh_TW |
dc.date.accessioned | 2021-05-20T19:59:08Z | - |
dc.date.available | 2016-10-03 | |
dc.date.available | 2021-05-20T19:59:08Z | - |
dc.date.copyright | 2011-10-03 | |
dc.date.issued | 2011 | |
dc.date.submitted | 2011-08-18 | |
dc.identifier.citation | Bahar, G., Feinmesser, R., Shpitzer, T., Popovtzer, A., and Nagler, R.M. (2007). Salivary analysis in oral cancer patients. Cancer 109, 54-59.
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/8636 | - |
dc.description.abstract | 口腔腫瘤內慢性發炎微環境中包括特定細菌族群,免疫細胞的浸潤以及發炎反應皆會影響到口腔癌細胞。但是細菌與口腔癌發炎環境相關性則尚未釐清。本研究主要建立細菌與口腔癌細胞株共同培養模式,探討口腔癌中口腔鏈球菌Streptococcus oralis以及Streptococcus mitis對口腔癌發炎環境所造成之影響。經由高劑量的細菌刺激之後,口腔癌細胞會產生高量的活性氧化物並導致細胞死亡。另一方面,在經由低劑量細菌或細菌細胞壁相關蛋白刺激之後,口腔癌細胞會增加促進腫瘤惡化、免疫細胞趨化相關激素的表現,包含IL-8、MCP-1、CCL20以及CCL22。並且刺激過後的細胞培養液能引起人類單核球細胞和T淋巴球的趨化。為進一步探討細菌刺激口腔癌細胞的訊號傳遞路徑,細胞處理NF-κB的抑制劑BAY-11-7082後會抑制細菌刺激產生MCP-1,而IL-8的產生則不受影響。另一方面,細胞處理STAT3的抑制劑Cpd188以及WP-1034後會抑制細菌刺激產生IL-8,MCP-1則不受影響。實驗結果顯示細菌會透過不同的訊息傳遞路徑活化癌細胞。由實驗結果推測,在口腔癌組織表層,高量的細菌刺激引發癌細胞死亡,產生組織潰爛的病理現象。而在癌組織內部,較少量的細菌刺激癌細胞產生細胞激素以及細胞趨化因子,促進免疫細胞浸潤至腫瘤組織,並加強腫瘤微環境的發炎反應。 | zh_TW |
dc.description.abstract | In tumor microenvironment, the presence of special bacteria, inflammation, and immune cells infiltration significantly influence on oral cancer. However, the relationship of bacteria and oral cancer were not clear. In order to examine the interaction between Streptococcus oralis, Streptococcus mitis and oral cancer cells (OCCs), the in vitro co-culture system of the special streptococci with OCCs is established. At higher multiplicities of infection (MOI), the OCCs generate high levels of ROS leading to cell death. At lower MOI, streptococci-stimulated OCCs expressed IL-8、MCP-1、CCL20 and CCL22 transcript and secret IL-8 and MCP-1 protein which were involved with cancer progression and immune cell recruitment. The conditioned medium from streptococci-stimulated OCCs had the ability to chemotaxis of human monocytic and T cells. MCP-1 was inhibited by NF-κB inhibitor BAY-11-7082 and IL-8 was inhibited by STAT3 inhibitor Cpd188 and WP-1034 demonstrated that bacteria can activate OCCs through different pathways. These data implied that higher amount of bacteria present in superficial of tumor leading to tissues necrosis and ulceration. In deeper tumor, lower amount of bacteria stimulated cancer cells to secret cytokine/chemokines leading immune cell infiltration, and augment the inflammation response in tumor microenvironment. | en |
dc.description.provenance | Made available in DSpace on 2021-05-20T19:59:08Z (GMT). No. of bitstreams: 1 ntu-100-R98450014-1.pdf: 1914060 bytes, checksum: 8145612427eca6174cb7d3041e5db2ee (MD5) Previous issue date: 2011 | en |
dc.description.tableofcontents | Content
Abstract in Chinese I Abstract in English II Chapter 1: Introduction 1 1.1 Oral Cancer 1 1.2 Relationship of Bacteria and Cancer 1 1.3 Cancer and Inflammation 5 1.3.1 NF-κB and STAT3 6 1.3.2 Cytokine and Chemokines 10 1.4 Reactive Oxygen Species 13 Chapter 2: Purposes and Aim 15 Chapter 3: Materials and Methods 16 3-1 Cell culture 16 3-1-1 Human Oral Cancer Cell line, Human Mononuclear Cell line 16 3-1-2 Preparation of Peripheral Blood Mononuclear Cells (PBMCs) 16 3-1-3 Normal Human Oral Keratinocytes (NHOK) 17 3-2 Interaction of Bacteria and Cells 17 3-2-1 Bacteria Culture and Preparation 17 3-2-2 Stimulation by Bacteria or Bacterial Cell-Wall-Associated Protein 18 3-3 Morphologic Analysis 19 3-4 Cell Cycle Assay 19 3-5 Apoptotic Cell Death Assay 20 3-6 RNA Extraction 20 3-7 Reverse Transcription 21 3-8 Polymerase Chain Reaction (PCR) and Real-time PCR 22 3-9 Enzyme-Linked Immunosorbent Assay (ELISA) 22 3-10 Chemotaxis Assay of PBMC and Monocytes 23 3-11 Preparation of whole cell lysates, cytosolic and nuclear extracts 23 3-12 Western blotting 24 3-13 Measurement of Reactive Oxygen Species 24 3-14 Statistical analysis 25 Chapter 4: Results 26 4.1 ROS Production by S. oralis, S. mitis and S. mutans-Stimulated Oral Cancer Cells 26 4.2 Expression of DNA Damage Marker γ-H2AX in Oral Cancer Cells after S. oralis and S. mitis Stimulation 26 4.3 Induction of Cell Death in Oral Cancer Cells after S. oralis and S. mitis Stimulation 27 4.4 Diphenyleneiodonium Inhibited Reactive Oxygen Species Production and Cell Death caused by S. oralis and S. mitis Stimulation 27 4.5 Cytokine Production in Oral Cancer Cell with S. oralis and S. mitis Stimulation 28 4.6 Cytokine Production in Oral Cancer Cell after S. oralis and S. mitis Cell-Wall-Associated Protein Stimulation 28 4.7 S. oralis and S. mitis-Stimulated Oral Cancer Cells Promote the Chemotaxis of Monocytes and T lymphocytes 29 4-8 S. oralis and S. mitis Cell-Wall-Associated Protein Stimulate Oral Cancer Cells Cytokine Production through NF-κB and STAT3 Pathways 30 4.9 Cytokine Production in Normal Human Oral Keratinocyte (NHOK) after S. oralis and S. mitis Cell-Wall-Associated Protein Stimulated 31 Chapter 5: Discussion 32 Chapter 6: References 38 Chapter 7: Tables 53 Chapter 8: Figures 54 | |
dc.language.iso | en | |
dc.title | 口腔鏈球菌引發人類口腔癌細胞死亡及發炎反應 | zh_TW |
dc.title | Cell Death and Inflammatory Response of Human Oral Cancer Cells Induced by Oral Streptococci | en |
dc.type | Thesis | |
dc.date.schoolyear | 99-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 黃敏銓,王萬波 | |
dc.subject.keyword | 細胞死亡,發炎反應,人類口腔癌細胞,口腔鏈球菌, | zh_TW |
dc.subject.keyword | Cell Death,Inflammatory Response,Human Oral Cancer Cells,Oral Streptococci, | en |
dc.relation.page | 65 | |
dc.rights.note | 同意授權(全球公開) | |
dc.date.accepted | 2011-08-18 | |
dc.contributor.author-college | 牙醫專業學院 | 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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