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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 胡孟君(Meng-Chun Hu) | |
| dc.contributor.author | Chih-Hung Chen | en |
| dc.contributor.author | 陳稚鴻 | zh_TW |
| dc.date.accessioned | 2021-07-11T15:14:40Z | - |
| dc.date.available | 2024-08-28 | |
| dc.date.copyright | 2019-08-28 | |
| dc.date.issued | 2019 | |
| dc.date.submitted | 2019-07-29 | |
| dc.identifier.citation | Brinkmann, A.O. (2011). Molecular mechanisms of androgen action--a historical perspective. Methods Mol Biol 776, 3-24.
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/78722 | - |
| dc.description.abstract | Interlukin-4 (IL-4) 是一種由T helper 2 細胞所分泌的細胞激素，調控T helper 2 細胞分化與增生。過去文獻發現IL-4能夠促進癌細胞的生長，包括乳癌、前列腺癌等癌細胞，並且影響癌細胞的生長以及轉移能力。本論文我們利用MTT試驗發現，在缺乏血清的情況下，IL-4促進HT-29大腸癌細胞的生長。利用群落生成分析IL-4對於細胞生長的影響，結果顯示IL-4能增加HT-29細胞群落生長的數目。遷移與侵入在癌細胞的轉移中扮演重要角色，wound healing試驗的結果顯示，IL-4會促進HT-29細胞遷移的能力，並且促進上皮間質轉化相關基因表現。此外，我們也發現IL-4調控了HT-29大腸癌細胞許多黏液素以及促發炎細胞激素基因的表現。先前我們的研究發現在HT-29細胞中，IL-4會誘導類固醇荷爾蒙生成基因HSD3B1的大量表現，並能促進HT-29細胞產生具生物活性的糖類皮質素。已知糖類皮質素會促進T細胞的凋亡。我們將老鼠脾臟細胞培養於HT-29細胞培養液中，並利用流式細胞儀進行細胞凋亡分析，發現經IL-4處理的HT-29細胞培養液培能促進T細胞的凋亡，說明IL-4可能經由HSD3B1的表現，促進HT-29糖類皮質素產生而促進T細胞的凋亡。進一步研究表觀遺傳學是否調控IL-4誘導的HSD3B1表現，我們發現廣效型組蛋白去乙醯化蛋白酶 (HDAC)抑制劑能有效降低IL-4所誘導之HSD3B1表現，甲基轉移酶抑制劑則沒有明顯效應，說明組蛋白去乙醯化蛋白酶的活性對於IL-4所誘導之HSD3B1表現可能是重要的。將細胞中的HDAC1、HDAC2或HDAC3 進行knockdown後，能夠抑制IL-4所誘導之HSD3B1表現，說明HDAC對於IL-4所誘導HSD3B1表現是重要的。然而，探討其可能的作用機制，實驗結果顯示HDAC抑制劑不會改變HDAC1、HDAC2、HDAC3以及HDAC4的表現量，不會影響IL-4兩個重要訊息傳遞路徑STAT6與AKT之活化，也不會影響IL-4所誘導之STAT6與HSD3B1啟動子的結合。綜合以上結果顯示，IL-4會促進大腸癌細胞HT-29的生長與遷移，以及促進HSD3B1的表現產生糖類皮質素而影響免疫反應。 | zh_TW |
| dc.description.abstract | Interleukin-4 (IL-4) is a cytokine secreted by T helper 2 cells which controls the differentiation and proliferation of T helper 2 cells. It has been demonstrated that IL-4 promotes cancer cell growth and metastasis, including breast cancer and prostate cancer. Here we showed that IL-4 stimulated HT-29 colon cancer cells growth under serum free condition measured by MTT assay. Besides, colony formation assay was performed to investigate the effects of IL-4 on the clonogenicity of HT-29 cells. Results showed that IL-4 promoted the ability of colony formation. Migration and invasion play a critical role in cancer metastasis. We further showed that IL-4 promoted the migration ability measured by wound healing assay and upregulated epithelial-mesenchymal transition-associated genes expression in HT-29 cells. We also found that IL-4 altered the expression of mucin genes and pro-inflammatory cytokines. Our previous study found that IL-4 induced steroidogenic gene HSD3B1 expression and stimulated bioactive glucocorticoids (GCs) production in HT-29 cells. It is known that GCs promote T cells apoptosis. Using flow cytometry analysis, we found that conditioned medium from HT-29 cells treated with IL-4 induced murine splenic T cells apoptosis, suggesting that IL-4 stimulated the production of GCs and promoted the T cells apoptosis, probably through the induction of HSD3B1 expression. To further investigate whether the epigenetic modifications are involved in IL-4-induced HSD3B1 expression. We found that IL-4-induced HSD3B1 expression was abolished by several HDAC inhibitors; however, the methyltransferase inhibitor had no significant effects. We further found HDAC1, HDAC2, or HDAC3 knockdown attenuated IL-4-induced HSD3B1 protein expression, indicating that these HDACs are critical for IL-4-induced HSD3B1 expression in HT-29 cells. IL-4 had no significant effects on HDAC1, HDAC2, HDAC3, and HDAC4 proteins expression, the phosphorylation of IL-4 downstream signaling STAT6 and AKT, and the ability of IL-4-induced STAT6 binding to HSD3B1 promoter. In summary, our study indicates that IL-4 promotes HT-29 cancer cell growth, migration, and the immunoregulatory GCs synthesis via HSD3B1 induction. | en |
| dc.description.provenance | Made available in DSpace on 2021-07-11T15:14:40Z (GMT). No. of bitstreams: 1 ntu-108-R06441005-1.pdf: 2171879 bytes, checksum: ed3361a0dbb97b61e72c4181daa6770a (MD5) Previous issue date: 2019 | en |
| dc.description.tableofcontents | 誌謝 I
目錄 II 表次 V 圖次 VI 附圖 VIII 中文摘要 IX Abstract XI I. Introduction 1 A. Biological functions of IL-4 1 B. IL-4 signaling transduction 2 C. Steroid hormones 3 D. Human HSD3B genes 4 E. Intestinal glucocorticoid synthesis and physiological functions 6 F. Histone deacetylase (HDAC) 6 G. Aim of the study 8 II. Materials and methods 9 A. Drugs 9 誌謝 I 目錄 II 表次 V 圖次 VI 附圖 VIII 中文摘要 IX Abstract XI I. Introduction 1 A. Biological functions of IL-4 1 B. IL-4 signaling transduction 2 C. Steroid hormones 3 D. Human HSD3B genes 4 E. Intestinal glucocorticoid synthesis and physiological functions 6 F. Histone deacetylase (HDAC) 6 G. Aim of the study 8 II. Materials and methods 9 A. Drugs 9 B. Cell culture 9 C. Whole cell lysates extraction 10 D. Western blot analysis 11 E. RNA isolation 14 F. Real-time RT-PCR 14 G. shRNA knockdown 17 H. Preparation of conditioned medium 20 I. Apoptotic T cells analysis 20 J. MTT assay 21 K. Wound healing assay 22 L. Colony formation assay 22 M. Chromatin immunoprecipitation (ChIP) 23 N. Statistical analysis 27 III. Results 28 A. Effects of IL-4 on HT-29 cell growth and migration ability 28 B. Effects of IL-4 on epithelial-mesenchymal transition (EMT) in HT-29 cells 29 C. Effects of IL-4 on mucin genes expression 29 D. Effects of IL-4 on pro-inflammatory cytokine genes expression 30 誌謝 I 目錄 II 表次 V 圖次 VI 附圖 VIII 中文摘要 IX Abstract XI I. Introduction 1 A. Biological functions of IL-4 1 B. IL-4 signaling transduction 2 C. Steroid hormones 3 D. Human HSD3B genes 4 E. Intestinal glucocorticoid synthesis and physiological functions 6 F. Histone deacetylase (HDAC) 6 G. Aim of the study 8 II. Materials and methods 9 A. Drugs 9 B. Cell culture 9 C. Whole cell lysates extraction 10 D. Western blot analysis 11 E. RNA isolation 14 F. Real-time RT-PCR 14 G. shRNA knockdown 17 H. Preparation of conditioned medium 20 I. Apoptotic T cells analysis 20 J. MTT assay 21 K. Wound healing assay 22 L. Colony formation assay 22 M. Chromatin immunoprecipitation (ChIP) 23 N. Statistical analysis 27 III. Results 28 A. Effects of IL-4 on HT-29 cell growth and migration ability 28 B. Effects of IL-4 on epithelial-mesenchymal transition (EMT) in HT-29 cells 29 C. Effects of IL-4 on mucin genes expression 29 D. Effects of IL-4 on pro-inflammatory cytokine genes expression 30 E. Effects of IL-4 on murine splenic T cells apoptosis 30 F. HDAC inhibitors abolish the IL-4-induced HSD3B1 expression in HT-29 cells 31 G. HDACs proteins expression are not affected by IL-4 in HT-29 cells 32 H. HDAC1, HDAC2 and HDAC3 are involved in IL4-induced HSD3B1 expression 33 I. IL-4 signaling pathways are not interrupted by HDAC inhibitors 34 J. Effects of IL-4 and HDAC inhibitor on STAT6 binding on HSD3B1 promoter in HT-29 cells 34 K. Effects of IL-4 and TSA on histone H3 acetylation on HSD3B1 promoter in HT-29 cells 35 IV. Discussion 36 A. Potential roles of IL-4 in HT-29 colon cancer cell growth and metastasis 36 B. The roles of IL-4 on intestinal GCs synthesis, immune regulation, and cytokines expression 38 C. Effects HDAC inhibitor on IL-4-induced HSD3B1 expression 39 V. References 42 | |
| dc.language.iso | en | |
| dc.subject | 大腸癌 | zh_TW |
| dc.subject | 介白素-4 | zh_TW |
| dc.subject | 組蛋白去乙醯化蛋白? | zh_TW |
| dc.subject | HSD3B1 | zh_TW |
| dc.subject | HSD3B1 | en |
| dc.subject | Interleukin-4 | en |
| dc.subject | colon cancer | en |
| dc.subject | Histone deacetylase | en |
| dc.title | Interleukin-4對於HT-29大腸癌細胞生長與轉移之影響 | zh_TW |
| dc.title | Interleukin-4 influences HT-29 colon cancer cell growth and metastasis | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 107-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 盧主欽(Juu-Chin Lu),張淑芬(Shwu-Fen Chang),徐立中(Li-Chung Hsu) | |
| dc.subject.keyword | 介白素-4,組蛋白去乙醯化蛋白?,HSD3B1,大腸癌, | zh_TW |
| dc.subject.keyword | Interleukin-4,Histone deacetylase,HSD3B1,colon cancer, | en |
| dc.relation.page | 66 | |
| dc.identifier.doi | 10.6342/NTU201902128 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2019-07-30 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 生理學研究所 | zh_TW |
| dc.date.embargo-lift | 2024-08-28 | - |
| 顯示於系所單位： | 生理學科所 | |
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