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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 潘建源 | |
| dc.contributor.author | Yu-Yin Shih | en |
| dc.contributor.author | 施鈺瑩 | zh_TW |
| dc.date.accessioned | 2021-06-17T00:31:21Z | - |
| dc.date.available | 2017-03-19 | |
| dc.date.copyright | 2012-03-19 | |
| dc.date.issued | 2012 | |
| dc.date.submitted | 2012-02-10 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/66347 | - |
| dc.description.abstract | 神經母細胞瘤是一種源自胚胎神經脊中交感神經前驅細胞為最常見的兒童時期腦外實心腫瘤。大多數的孩童在被診斷時疾病已處於晚期或是為轉移的型態。有些轉移的腫瘤能藉由分化或凋亡自行退化或發展成良性的神經節細胞瘤。在先前的研究中我們已鑑定葡萄糖調控蛋白(GRP75)與鈣網絡蛋白(CRT)涉及神經母細胞瘤分化被當作神經母細胞瘤的診斷因子。然而，葡萄糖調控蛋白及鈣網絡蛋白於神經母細胞瘤分化的機制還未明瞭。於現今第一部分的研究中我們證實葡萄糖調控蛋白能和維甲酸細胞核alpha受體(RARα)及類視黃醇alpha受體(RXRα)形成綜合體去調控維甲酸引起的神經分化。葡萄糖調控蛋白藉由增加維甲酸細胞核alpha受體及類視黃醇alpha受體的蛋白質穩定度調控維甲酸細胞核alpha受體及類視黃醇alpha受體的反式激活作用。第二部份的研究我們鑑定鈣網絡蛋白藉由它的鈣調節功能參與在神經生長因子促使的分化中。大量表現鈣網絡蛋白能向上調節MAPK信號傳遞促進神經生長因子引起的分化及藉由向下調控Akt路徑產生凋亡。此外，鈣網絡蛋白能調控MYCN的表現量於轉錄程度。整體而言，我們的研究結果提供了基礎於未來設計新的增進神經母細胞瘤病患存活率的治療策略。 | zh_TW |
| dc.description.abstract | Neuroblastoma (NB) is the most common extracranial solid tumor of children and is originated from primitive sympathetic neural precursors derived from neural crest. Most children have advanced or metastatic status of disease at diagnosed age. Some of these metastatic tumors can spontaneously regress or mature into a benign ganglioneuroma by undergoing differentiation or apoptosis. In previous research, we have identified that glucose-regulated protein 75 (GRP75) and calreticulin (CRT) were the factors that involved in neuroblastoma differentiation as the prognostic indicator for NB. However, the mechanisms underlying the GRP75 and CRT on neuronal differentiation of NB remain elusive. In the first part of present studies, we have demonstrated that GRP75 could form a complex with retinoic acid receptor alpha (RARα)/rexinoid receptor alpha (RXRα) to modulate retinoic acid (RA)-elicited neuronal differentiation. The transactivation of RARα/RXRα was regulated by GRP75 through increasing the protein stability of RARα/RXRα. In the second part, we identified that CRT participated in nerve growth factor (NGF)-induced differentiation by its Ca2+ buffering function. Overexpression of CRT promoted NGF-mediated differentiation by upregulation mitogen-activated protein kinase (MAPK) signaling and induced apoptosis through downregulation Akt pathway. Furthermore, CRT regulated v-myc myelocytomatosis viral related oncogene (MYCN) expression at the transcriptional level. Collectively, our data provide the basis for designing new therapeutic strategies to improve survival rate of NB patients in the future. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-17T00:31:21Z (GMT). No. of bitstreams: 1 ntu-101-D95b41006-1.pdf: 8242739 bytes, checksum: 1066d8c9577a09586a281480af5f21a9 (MD5) Previous issue date: 2012 | en |
| dc.description.tableofcontents | Table of Contents
誌謝 I 中文摘要 II Abstract III Table of Contents 1 List of Figures 5 List of Tables 8 Part I Introduction 9 Neuroblastoma 10 Neuroblastoma 10 Clinical features of neuroblastoma 10 Prognosis 11 MYCN amplification 12 Treatment 13 Neuronal Differentiation 14 Molecular mechanisms governed neuronal differentiation of neuroblastoma 14 Retinoic acid (RA) 16 Nerve growth factor (NGF) 19 Advance research of neuroblastoma in the future 20 Chaperones 20 Chaperones in Cancer 22 Glucose-regulated protein 75 (GRP75) 22 Calreticulin (CRT) 24 Part II Nuclear GRP75 modulates RA-elicited neuroblastoma differentiation through interaction with retinoic acid receptors 26 Abstract 27 Materials and Methods 28 Cell culture and patient samples 28 Reagents and antibodies 28 Immunofluorescence confocal microscopy 28 Plasmids, transfection, and retroviral infection 29 Immunoprecipitation and Western blot 30 EMSA 33 Luciferase reporter assay 33 Quantitative real-time RT-PCR 34 Chromatin immunoprecipitation (ChIP) 34 Ubiquitination assay 35 Tumor growth in nude mice 36 Statistical analysis 36 Results 38 GRP75 presents in nucleus 38 GRP75 interacts with retinoic acid receptors in neuroblastoma cells 39 Down-regulation of GRP75 inhibits RA-elicited activation of RARα/RXRα | |
| dc.language.iso | en | |
| dc.subject | 神經生長因子 | zh_TW |
| dc.subject | 神經母細胞瘤 | zh_TW |
| dc.subject | 葡萄糖調控蛋白 | zh_TW |
| dc.subject | 鈣網絡蛋白 | zh_TW |
| dc.subject | 神經分化 | zh_TW |
| dc.subject | 維甲酸 | zh_TW |
| dc.subject | Neuroblastoma | en |
| dc.subject | NGF | en |
| dc.subject | Retinoic acid | en |
| dc.subject | Neuronal differentiation | en |
| dc.subject | CRT | en |
| dc.subject | GRP75 | en |
| dc.title | 葡萄糖調控蛋白與鈣網絡蛋白於神經母細胞瘤分化的角色 | zh_TW |
| dc.title | The Roles of Glucose-Regulated Protein 75 and Calreticulin
in Neuronal Differentiation of Neuroblastoma | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 100-1 | |
| dc.description.degree | 博士 | |
| dc.contributor.coadvisor | 廖永豐 | |
| dc.contributor.oralexamcommittee | 李心予,許文明,蔡有光 | |
| dc.subject.keyword | 神經母細胞瘤,葡萄糖調控蛋白,鈣網絡蛋白,神經分化,維甲酸,神經生長因子, | zh_TW |
| dc.subject.keyword | Neuroblastoma,GRP75,CRT,Neuronal differentiation,Retinoic acid,NGF, | en |
| dc.relation.page | 164 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2012-02-13 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 動物學研究所 | zh_TW |
| 顯示於系所單位： | 動物學研究所 | |
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