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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 陳美如 | |
| dc.contributor.author | Yu-Bo Zou | en |
| dc.contributor.author | 鄒宇博 | zh_TW |
| dc.date.accessioned | 2021-07-11T15:18:07Z | - |
| dc.date.available | 2024-08-28 | |
| dc.date.copyright | 2019-08-28 | |
| dc.date.issued | 2019 | |
| dc.date.submitted | 2019-07-17 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/78770 | - |
| dc.description.abstract | Epstein-Barr virus (EBV) is a human gamma-herpesvirus. Previous studies of nasopharyngeal carcinoma (NPC) serology indicates that recurrent EBV reactivation is highly correlated with NPC development and in the mouse xenograft model, recurrent EBV reactivation was demonstrated to increase tumorigenicity and metastasis ability of cell. Among viral lytic proteins, EBV DNase was reported to induce host cell genome instability and potentially increases tumorigenicity of NPC cells. Considering that other lytic proteins also have potential oncogenic function, we investigated further about the potential oncogenic role of BGLF4 during virus recurrent reactivation in NPC cells. EBV BGLF4 is a serine/threonine protein kinase that has a broad-spectrum viral and cellular substrates. At the late stage of virus replication, BGLF4 induces partial nuclear lamina disassembly through a cellular CDK1-mimicking pathway. In addition, BGLF4 induces nucleus shape alteration and cytoskeleton rearrangement. Considering the regulatory role of nucleus and cytoskeleton in cell migration, we adopt inverted transwell and boyden chamber with different pore size to examine the influence of repetitive BGLF4 expression on cell invasiveness and motility. We demonstrate that repetitive expression of BGLF4 increases invasiveness and motility of NPC-TW01 cells. Also, repetitive BGLF4 expression contributes to a loosen nuclear lamina in cells and hence promotes cell migrates through a narrow space in a size smaller than the cell nucleus. Moreover, BGLF4 redistributes E-cadherin and induces F-actin protrusion formation at cell margin which may contribute to cell migration in a 3D environment. In conclusion, we prove that repetitive BGLF4 expression increase cell invasiveness and motility that may promote tumor metastasis. | en |
| dc.description.provenance | Made available in DSpace on 2021-07-11T15:18:07Z (GMT). No. of bitstreams: 1 ntu-108-R06445136-1.pdf: 25362571 bytes, checksum: b834a78a1531eb74e3f9ef43159dbc90 (MD5) Previous issue date: 2019 | en |
| dc.description.tableofcontents | 口試委員審定書 I
致謝 II 摘要 III ABSTRACT IV 1. INTRODUCTION 1 1.1. Epstein-Barr virus (EBV) 1 1.1.1. Classification and Characterization of EBV 1 1.1.2. EBV latency and associated diseases 1 1.2. Oncogenicity of EBV 2 1.2.1 Tumorigenic function of latent infection and latent proteins 2 1.2.2 EBV reactivation and NPC 3 1.2.3EBV reactivation and tumorigenic function of lytic proteins 4 1.3. Conserved Herpes protein kinase (CHPK) 4 1.3.1 Characterization of CHPK 4 1.3.2 EBV protein kinase BGLF4 5 1.4. Nuclear rigidity and cancer metastasis 6 1.4.1 Obstacles for cancer cell metastasis 6 1.4.2 The role of nuclear lamina and nucleus stiffness in cancer cell metastasis 7 1.5. E-cadherin and metastasis 8 1.5.1 General function of E-cadherin 8 1.5.2 The role E-cadherin in tumor metastasis 9 1.6. Specific Aims 10 2. MATERIALS & METHODS 11 2.1. Cell culture 11 2.2. Inverted transwell assay 12 2.3. Transwell assay 12 2.4. Cell transfection 13 2.5. Western blot analysis 13 2.6. Immunofluorescence assay (IFA) 14 2.7. Quantitative polymerase chain reaction (Q-PCR) analysis 15 3. RESULTS 16 3.1. Repetitive induction of BGLF4 in TW01 promotes cell invasiveness and motility 16 3.2. Repetitive BGLF4 expression contribute to nuclear lamina deformation 17 3.3. Repetitive BGLF4 expression in TW01 promotes cell migration ability through narrow space without reducing Lamin A/C expression 17 3.4. BGLF4 disrupt E-cadherin distribution at the adherent junction 18 3.5. E-cadherin expression is not directly regulated by BGLF4 19 4. DISCUSSION 20 5. FIGURES 24 Fig. 1. Schematic diagram of repetitive induction of BGLF4. 24 Fig. 2. Repetitive expression of BGLF4 promotes cell invasiveness in TW01. 25 Fig. 3. Repetitive induction of BGLF4 in Tet- on BGLF4 TW01 promotes cell motility. 26 Fig. 4. Repetitive expression of BGLF4 in Tet-on BGLF4 TW01 induces nuclear lamina partial disassembly. 27 Fig. 5. Repetitive expression of BGLF4 induces nuclear lamina deformation. 28 Fig. 6. Repetitive induction of BGLF4 in Tet-on BGLF4 TW01 promotes cell motility through narrow space. 29 Fig. 7. Repetitive induction of BGLF4 in Tet-on BGLF4 TW01 induce neither significant p-Lamin A/C s22 phosphorylation nor decreasing of Lamin A/C. 30 Fig. 8. Effect of BGLF4 in regulating E-cadherin distribution in adherent junction among Tet-on BGLF4 TW01 cells. 31 Fig. 9. BGLF4 expression disrupts the linear distribution of E-cadherin in KIT2 and KIT20. 32 Fig. 10. BGLF4 down-regulates MMP9 mRNA level but not E-cadherin. 33 Fig. 11. Transient transfection of BGLF4 increases F-actin protrusion number in the cell margin of TW01. 34 Fig. 12. Repetitive BGLF4 expression do not promote 2D migration. 35 6. REFERENCES 36 | |
| dc.language.iso | en | |
| dc.subject | 細胞侵襲 | zh_TW |
| dc.subject | 細胞移動 | zh_TW |
| dc.subject | EB病毒 | zh_TW |
| dc.subject | EBV | en |
| dc.subject | cell migration | en |
| dc.subject | cell invasion | en |
| dc.title | NPC-TW01中的BGLF4重複表達提升細胞侵襲和移動能力 | zh_TW |
| dc.title | Repetitive BGLF4 expression promotes NPC-TW01 cell invasiveness and motility | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 107-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 張智芬,李明學,李重霈 | |
| dc.subject.keyword | EB病毒,細胞移動,細胞侵襲, | zh_TW |
| dc.subject.keyword | EBV,cell invasion,cell migration, | en |
| dc.relation.page | 41 | |
| dc.identifier.doi | 10.6342/NTU201901566 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2019-07-17 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 微生物學研究所 | zh_TW |
| dc.date.embargo-lift | 2024-08-28 | - |
| 顯示於系所單位： | 微生物學科所 | |
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