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研究生:劉祐君
研究生(外文):Yu-Chun Liu
論文名稱:利用賀爾蒙及免疫系統調控子宮內膜及卵巢癌細胞的細胞外間質分子
論文名稱(外文):Regulation of ECM molecules in endometrium and ovarian cancer cell by hormone and immune systems
指導教授:王妙媛王妙媛引用關係
指導教授(外文):Nancy M. Wang
學位類別:碩士
校院名稱:國立彰化師範大學
系所名稱:生物技術研究所
學門:生命科學學門
學類:生物科技學類
論文種類:學術論文
論文出版年:2011
畢業學年度:99
語文別:英文
論文頁數:88
中文關鍵詞:子宮內膜異位症卵巢癌細胞外間質
外文關鍵詞:endometriosisovarian cancerextracellular matrix (ECM)
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子宮內膜異位症及卵巢癌皆具有增生、發炎反應及受hormone調控的病理機制。細胞外間質 (ECM molecules) 調控著細胞的黏附、增生和侵入,在子宮內膜異位症及卵巢癌的致病機轉皆扮演著很重要的角色。先前研究中發現,細胞外間質TIMP-2, VCAM-1和 VTN在子宮內膜異位症及卵巢癌具有不一樣的表現,此差異可能受到hormone和immune systems所調控。因此本研究主要目的是建立細胞株研究模式 (OVA, ovarian cancer cell line; EM, endometriotic cell line; NEM, endometrial cell lines) 來探討這兩種疾病中的ECM molecules如何受到hormone和immune systems所調控。EM及OVA cell lines中ECM molecules (TIMP-2, VCAM-1和 VTN)TIMP-2,VCANM-1在EM中表現各高於OVA 4.13-fold , 20.06-fold ,相反的VTN 在OVA中表現高於EM 27.17-fold。除此之外,比較EM及OVA的ESR1/ESR2的ration值,EM的ration值為0.05而OVA的ration值為0.007。研究指出,IL-6會與許多其他cytokines刺激VTN表現,而TNF-α則增加VCAM-1的表現且cytokines皆會促進cell migration及cell proliferation。在hormone方面,E2及P4會藉由降低NF-κB-mediated transcriptional的活性減少VCAM-1的表現,增加MMP-2的活性改變與TIMP-2之間的平衡而降低TIMP-2的表現,除此之外還會降低VTN的表現。Hormone皆會減少cell migration及增加cell proliferation。因此我們推測,IL-6及TNF-α會促進VTN及 VCAM-1的表現並促進細胞的migration及proliferation而增加子宮內膜異位症的development。可利用CD34 及HOXA10的biomarker測定子宮內膜異位症的development。當子宮內膜異位組織轉移至卵巢時,hormone會促使TIMP-2表現減少及angiogenesis和invasion的產生,而增加卵巢癌的development。可利用VSGP/F-spondin及Keratin19的biomarker測定卵巢癌的development 。Cytokines持續刺激會增加VTN的表現讓細胞有metastasis的能力。
Cell adhesion and invasion both play important roles in the pathogenesis of endometriosis and ovarian cancer through ECM molecules. Previous study has found differential expressions of TIMP-2, VCAM-1and VTN between endometriotic tissues and ovarian cancer which may be under controlled of hormone and immune systems. Thus, a putative pathogenic regulation model of these two diseases by ECM molecules was hypothesized. The aim of this study is to verify this hypothesis in an in vitro model. Expressions of ECM molecules and hormone receptor in (EM) and (OVA) cell lines that TIMP-2 and VCAM-1 expressed 4.13-fold and 20.06-fold higher respectively in endometriotic cell than ovarian cancer cell but expression of VTN was increased 27.17-fold in ovarian cancer. Besides, the ration of ESR1 / ESR2 to compare in endometriotic cell and ovarian cancer that indicated the ration of ESR1 / ESR2 was 0.05 in endometriotic cell and the ration of ESR1 / ESR2 was 0.007 in ovarian cancer. In our study, up-regulations of VCAM-1, VTN and down-regulation TIMP-2 increased in the pathogenesis. In immune system, IL-6 stimulates VTN expression with IL-11 and LIF; TNF-α induces expression of VCAM-1. The cytokine can increase cell migration and cell proliferation. In hormone system, E2 and P4 decreased VCAM-1 expression with directly suppression of NF-κB-mediated transcriptional activation. E2 and P4 decreased expression of TIMP-2 by expression of MMP-2. The hormone can decrease cell migration and increase cell proliferation. We proposed that up-regulations of VTN , VCAM-1 increased cell migration and cell proliferation by IL-6 and TNF-α may be increased in the risk of endometriosis. The CD34 and HOXA10 of biomarker can confirm development of endometriosis. The endometriotic tissue in the ovary that down-regulations of TIMP-2 than decrease cell migration and increase cell proliferation by hormone may be increased in the risk of ovarian cancer. However, the hormone increased angiogenesis of endometriotic tissue by expression of VEGF. The VSGP/F-spondin and Keratin19 of biomarker can confirm development of ovarian cancer. Up-regulations of VTN may be increased cell metastasis.
Content
Page
Abstract I
Abstract (Chinese) II
Acknowledgement III
Content IV
Chapter 1 Introduction 1
1. Extracellular matrix 1
1.1 ECM in endometriosis 1
1.2 ECM in ovarian cancer 2
2. Expression of TIMP-2, VCAM-1 and VTN in endometriosis and ovarian cancer 3
2.1 TIMP-2 3
2.2 VCAM-1 4
2.3 Vitronectin 5
3. Hormone effect ECM molecules 5
3.1 Hormone effect ECM molecules in endometriosis 5
3.2 Hormone effect ECM molecules in ovarian cancer 7
4. Cytokine effect ECM molecules 7
4.1 Cytokine effect ECM molecules in endometriosis 7
4.2 Cytokine effect ECM molecules in ovarian cancer 8
5. Specific aim 9
Chapter 2 Materials and methods 10
1. Experimental procedures 10
2. Cell culture 11
3. Cell treatment 12
4. RNA extraction 12
5. Reverse transcription PCR 13
6. Real-time PCR 13
7. Cell proliferation with MTT (3-[4,5-dimethythiazol-2-yl-)-2,5-diphenyl tetrazolium bromide]) 15
8. Cell migration (wound healing assay) 16
Chapter 3 Result 18
1. The differential expression of hormone receptor and ECM molecules in endometri- osis and ovarian cancer 18
2. Exam pathogenesis of endometriosis and ovarian using a cell-base model to determine the hormonal and cytokine affects on ECM molecules 19
3. Cytokines (IL-6 and TNF-α) increased expression of VTN and VCAM-1 20
4. Hormone (estrade and progesterone) decreased expression of ECM molecules 21
5. Cytokines (IL-6 and TNF-α) affected expression of hormone receptor 22
6. Hormone (estrade and progesterone) affected expression of hormone receptor 24
7. Cytokines (IL-6 and TNF-α) increased cell migration fold 25
8. Hormone (estrade and progesterone) decreased cell migration fold 26
9. Cytokines and hormone increased cell proliferation 26
10. Cytokines (IL-6 and TNF-α) affect expression of VTN and VCAM-1, but not hormone receptor in endometriotic cell (EM) 27
11. Hormone (estrade and progesterone) decreased expression of ECM molecules in endometriotic cell (EM) 28
Chapter 4 Discussion 29
1. The differential ECM molecules regulated development of endometriosis and ovarian cancer 29
2. Expression of hormone receptor the pathogenesis of endometriosis or ovarian
cancer 31
3. Cytokines and hormone can affect expression ECM molecules in endometrial cell and increased pathogenesis of endometriosis 32
4. Hormone can affect expression hormone receptor in endometrial cell but not cytokine 35
5. Cytokine can affect cell migration and cell proliferation and increased pathogenesis of endometriosis 36
6. Immune system regulated expression of ECM molecules and increased pathogenesisof endometriosis and ovarian cancer 37
Chapter 5 References 39
Chapter 6 Tables 48
1. Oligonucleotide primer pairs of ESR1, ESR2, PGR and RPS18 for real-time PCR analysis 48
2. Oligonucleotide primer pairs of TIMP-2, VCAM-1, VTN and ACTB for real-time PCR analysis. 49
3. ECM molecules gene expression comparison between EM and OVA 50
4. Hormone receptor gene expression comparison between EM and OVA 51
5. IL-6 affect expression of VCAM-1 and VTN but not affect hormone receptor in EM 52
6. TNF-α affect strong expression of VCAM-1 but not affect hormone receptor in EM 53
7. Estrade decreased expression of VCAM-1 and VTN but not affect hormone receptor in EM 54
8. Progesterone decreased expression of VCAM-1 and VTN and increased ESR2 expression in EM 55
Chapter 7 Figures 56
1. Differential regulation of ECM molecules via hormone and immune systems in endometriosis and ovarian cancer 56
2. Fold of ECM molecules expression to compare endometriotic cell and ovarian cancer 57
3. The ration of ESR1 / ESR2 to compare endometriotic cell and ovarian cancer 58
4. Fold of ECM molecules expression in endometrial cell with treatment different concentration of IL-6 in CSS 59
5. Fold of ECM molecules expression in endometrial cell with treatment different concentration of TNF-α in CSS. 60
6. Fold of ECM molecules expression in endometrial cell with treatment TNF-α and IL-6 in CSS 61
7. Fold of ECM molecules expression in endometrial cell with treatment different concentration of estrade in CSS 62
8. Fold of ECM molecules expression in endometrial cell with treatment different concentration of progesterone in CSS 63
9. Fold of hormone receptor expression in endometrial cell with treatment different
concentration of IL-6 in CSS 64
10. Fold of hormone receptor expression in endometrial cell with treatment different concentration of TNF-α in CSS 65
11. The ration of ESR1 / ESR2 to compare in endometrial cell with treatment TNF-α and IL-6 66
12. Fold of hormone receptor expression in endometrial cell with treatment different concentration of estrade in CSS 67
13. Fold of hormone receptor expression in endometrial cell with treatment different concentration of progesterone in CSS. 68
14. The ration of ESR1 / ESR2 to compare in endometrial cell with treatment estrade and progesterone 69
15. Cell migration of OVA, NEM and EM in picture 70
16. Cell migration fold of OVA, NEM and EM 71
17. Cytokines increase cell migration rate by culture in phenol-red-free media supplemented with CSS 72
18. Cytokines increase cell migration rate by culture in DMEM 73
19. Cytokines (TNF-α and IL-6) increase cell migration fold 74
20. Hormone decreased cell migration rate by culture in phenol-red-free media supplemented with CSS 75
21. Hormone decreased cell migration rate by culture in DMEM 76
22. Hormone decreased cell migration fold 77
23. The cell growth properties with TNF-α treatment in endometrial cell 78
24. The cell proliferation fold with TNF-α treatment in endometrial cell in 24 and 72 hr 79
25. The cell growth properties with IL-6 treatment in endometrial cell 80
26. The cell proliferation fold with IL-6 treatment in endometrial cell in 24 and 72 hr 81
27. The cell growth properties with estread treatment in endometrial cell. 82
28. The cell proliferation fold with estrade treatment in endometrial cell in 24hr and 72 hr 83
29. The cell growth properties with progesterone treatment in endometrial cell 84
30. The cell proliferation fold with progesterone treatment in endometrial cell in 24hr and 72hr 85
31. Model for the interaction of ECM molecules with endometrial cells in the pathogenesis of endometriosis 86
32. Hormone and immune systems differential regulate development of endometriosis and ovarian carcinoma by ECM molecules 88
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