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RUNX1T1調控內皮細胞分泌因子影響其細胞血管生成能力

為了解決異形蛋ro的問題，作者廖可熏 這樣論述：

近年來，研究發現內皮前驅細胞（EPCs）是調控腫瘤微環境的關鍵因子，也被當作缺血相關疾病的治療方法。內皮前驅細胞依賴其細胞的能力用來可以啟動血管新生的步驟，幫助組織再生和腫瘤進展期間的血管生成。雖然內皮前驅細胞的分泌因子參與在 EPC所調控的活動，但驅動其分泌蛋白表達的上游因子仍然不甚了解。在此研究中，抑制 RUNX1T1表達的 EPCs，降低了其細胞的存活率，移動及形成管狀之能力。在過度表現 RUNX1T1的 EPCs，發現其細胞能力有所增加。可證明 RUNX1T1可經由調控內皮前驅細胞的能力影響血管結構的恆定。此外，利用系統生物學方法，識別出 RUNX1T1所影響之基因特徵相較與卡波西肉

瘤皰疹病毒感染的內皮細胞的基因特徵，發現兩者所影響基因呈正相關，皆為促進內皮細胞血管生成能力之相關基因。在小鼠模型中，發現 RUNX1T1參與小鼠胚胎早期心血管發育形成所需的血管生成。剔除 RUNX1T1會造成小鼠的早期胚胎異常並死亡，在異形合子的小鼠身上也可發現血管結構不緊密造成物質滲漏的異常情形。根據 RUNX1T1影響的基因特徵，利用生物資訊分析後，發現血管內皮生長因子A (VEGFA)、骨塑型蛋白4 (BMP4) 和 轉化生長因子2 (TGF2) 是 RUNX1T1所調控的下游細胞分泌因子，並且在細胞及動物實驗中證明 RUNX1T1可調控這三種分泌蛋白進而調控前驅細胞的血管生成能力

及異型合子小鼠的血管生成。在此研究中證明， RUNX1T1是 EPC存活及維持其細胞功能所需的中心因子。因此， RUNX1T1有可能作為慢性心血管疾病調控的發展目標，或是抑制血管生成如癌症的潛在發展目標。

鼻咽癌中高度甲基化基因之研究

為了解決異形蛋ro的問題，作者彭宸璟 這樣論述：

Index指導教授推薦書 ............................................................................................................口試委員會審定書 .......................................................................................................中文摘要 .............................................................

......................................................... iiiAbstract ....................................................................................................................... ivIndex ......................................................................................................

........................ vFigures index .............................................................................................................. viTables index .............................................................................................................. viiiIntroduction ......

............................................................................................................ 11. Nasopharyngeal carcinoma and Epstein-Barr virus ........................................................... 12. DNA methylation and NPC ...................................................

............................................ 43. Homeobox gene ................................................................................................................. 54. Claudin................................................................................................................

.............. 7Specific aims ............................................................................................................... 12Materials and methods .............................................................................................. 13Results .............................

............................................................................................ 241. Molecular mechanisms of homeobox A2 gene (HOXA2) ............................................ 241.1 Differentially methylated HOXA2 correlates with low mRNA expression in NPCbiopsies and cell lines ....

.................................................................................................. 241.2 DNA methylation suppresses HOXA2 promoter activity by impairing the binding ofthe transcription activator, p300 ...................................................................................

... 261.3 Functional analysis of HOXA2-expressing NPC cell lines ....................................... 281.4 HOXA2 down-regulates MMP-9 expression and enzymatic activity ....................... 291.5 HOXA2 antagonizes TBP by binding to TATA-box and suppresses MMP-9transcription ...................

.................................................................................................. 301.6 HOXA2 methylation status positively correlates with EBV copy number and MMP-9levels in plasma from NPC patients ................................................................................ 33

2. Molecular mechanisms of claudin-11 gene (CLDN11) ................................................ 352.1 CLDN11 methylation status conversely correlates with mRNA expression in NPC 352.2 DNA methylation causes CLDN11 inactivation through interfering the binding ofGATAs toward CLDN11 promoter .....

............................................................................ 372.3 CLDN11 inhibits cell migration and invasion in NPC cells ..................................... 392.4 Identification of putative CLDN11 interacting proteins in NPC cells ...................... 39Discussion ............

........................................................................................................ 41Figures ......................................................................................................................... 50Tables ......................................................

.................................................................... 85References ................................................................................................................... 91Figures indexFigure 1. Hybridized signals of HOXA2 and IRF7 in 4-paired NPC samples inTranSignalTM m

ethylation promoter array ......................................... 50Figure 2. Identification of HOXA2 as the differentiated hypermethylated genein NPC by Sequenom Mass array ...................................................... 51Figure 3. Bisulfite sequencing analysis of HOXA2 promoter in NPC ..

.......... 52Figure 4. Quantitative methylation specific PCR analysis of HOXA2 promoterin NPC ................................................................................................ 53Figure 5. HOXA2 mRNA expression in NPC tissues and NPC cell lines ...... 54Figure 6. Correlation of HOXA2 m

ethylation status and RNA expression inNPC paired tumors ............................................................................. 55Figure 7. Patch methylation of HOXA2 promoter ........................................... 56Figure 8. Promoter activity analysis of HOXA2 in NPC cells ............

............ 57Figure 9. Chromatin immunoprecipitation analysis of the binding affinity ofp300 on HOXA2 promoter ................................................................ 58Figure 10. DNA pull-down analysis of p300 on HOXA2 promoter ................ 59Figure 11. Cell proliferation ability of

HOXA2 in HK1 and TW02 cells ....... 60Figure 12. Cell invasion ability of HOXA2 in HK1 and TW02 cells .............. 61Figure 13. Repressive effect of HOXA2 on MMP-9 in NPC cells .................. 62Figure 14. Transcriptional repressive effect of HOXA2 on MMP-9 promoter inNPC cells ................

........................................................................... 64Figure 15. Transcriptional repressive effect of HOXA2 and activated effect ofTBP on MMP-9 promoter in NPC cells ............................................. 65Figure 16. DNA pull-down analysis of HOXA2, TBP and RNA polyme

rase IIon MMP-9 promoter .......................................................................... 66Figure 17. EMSA analysis of HOXA2 and TBP binding affinity toward MMP-9 TATA box region ............................................................................ 67Figure 18. Chromatin immunoprec

ipitation analysis of the binding affinity ofHOXA2, TBP and RNA pol II on MMP-9 promoter ........................ 68Figure 19. Correlation of EBV copy number, HOXA2 methylation status andMMP-9 concentration in plasma samples from NPC patients ........... 70viiFigure 20. Schematic model of silencing

of the transcription repressor HOXA2by aberrant hypermethylation enhances invasion via MMP-9activation in NPC ............................................................................... 71Figure 21. Screening of differentially hypermethylated genes in NPC ........... 72Figure 22. Bisulfite seque

ncing analysis of CLDN11 promoter in NPC ......... 73Figure 23. CLDN11 expression in NPC tissues and NPC cell lines ................ 76Figure 24. Promoter activity analysis of CLDN11 in NPC cells ..................... 77Figure 25. Promoter activity analysis of CLDN11 with GATA binding sitesmutation

in NPC cells ........................................................................ 78Figure 26. DNA pull-down analysis of GATA on CLDN11 promoter ........... 79Figure 27. Cell proliferation ability of CLDN11 in TW02 and CNE1 cells .... 80Figure 28. Cell migration and invasion ability of CLDN11 in

NPC cells ....... 81Figure 29. Putative CLDN11 interacting proteins identified by LC MS/MSanalysis ............................................................................................... 82Figure 30. Protein-protein interaction of flag-tagged CLDN11 withendogenous TUBA1B and TUBB3 .........

.......................................... 83Figure 31. Proposed model of silencing of the tight junction gene CLDN11 byaberrant hypermethylation in nasopharyngeal carcinoma ................. 84Tables indexTable 1. Sequences for PCR primers ...........................................................

................ 85Table 2. Sequence for DNA pull-down and EMSA biotinylated primers ................... 86Table 3. EBV copy number, HOXA2 methylation percentage of cell-free DNA andMMP9 protein amount detected from five NPC patients’ plasma collected atdifferent time ...............................

....................................................................... 87Table 4. Expression of Claudins in human tumors (Turksen and Troy, 2011) ............ 88Table 5. Tight junction-related genes expression and methylation status in NPC ...... 90