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| 題名: | 探討ARID3B在缺氧狀態活化上皮間質轉化過程中扮演之角色
Investigating the role of ARID3B in hypoxia-induced epithelial-mesenchymal transition |
| 作者: | 謝杰恩
HSIEH, CHIEH-EN |
| 貢獻者: | 醫學科學研究所碩士班
廖彩岑 |
| 關鍵詞: | 結直腸癌;缺氧;上皮間質轉化
ARID3B;Colorectal cancer;Hypoxia;Epithelial-mesenchymal transition |
| 日期: | 2023-01-12 |
| 上傳時間: | 2023-12-15 14:05:58 (UTC+8) |
| 摘要: | 結直腸癌 (CRC) 是世界上最致命的癌症之一，並且結直腸癌的發病率逐年增加。儘管早期診斷和治療可提高長期生存率，但晚期結 直腸癌患者的預後仍然很差。上皮-間質轉化 (EMT) 在癌細胞侵襲和 表型轉移中有著關鍵作用，這也是結直腸癌晚期死亡率較高的原因。 此外，上皮-間質轉化還增強了癌症的幹性特徵。在結直腸癌中，富含 AT 相互作用結構域蛋白 3B (ARID3B) 已被證明是通過染色質重組 調節幹性特徵和免疫逃脫的重要因素。在這項研究中，我們旨在研究 結直腸癌中，ARID3B 在上皮-間質轉化過程扮演的角色。TCGA 分 析的數據還表明，上皮標記物(CDH1、JUP)和間質標記物(FN1、 VIM、Snail)都與ARID3B 呈現正相關，因此我們推測 ARID3B 可 能參與混合態上皮-間質轉化。實驗結果表明異位 ARID3B 表達可激 活上皮-間質轉化，而降低 ARID3B 的表達可逆轉上皮-間質轉化。先 前的研究已經證實，缺氧會促進上皮-間質轉化。有趣的是，結果表明 ARID3B 在缺氧模擬條件下會被激活，包括氯化鈷 (CoCl2) 處理和 1% O2 缺氧室培養。報導分析實驗還證實 HIF-1α 表達激活了 ARID3B 表達。此外，降低 AIRD3B 的表達會逆轉缺氧誘導的上皮 -間質轉化，結果表明 ARID3B 的表達可能與 HIF-1α 的穩定性有關， 這將在我們進一步的實驗中得到驗證。綜合以上我們的數據表明ARID3B 是 EMT 的關鍵介質，並參與了結直腸癌中缺氧誘導的上 皮-間質轉化。
Colorectal cancer (CRC) is one of the deadliest cancers in the world, and the incidence of CRC increases annually. Although early diagnosis and treatment increase long-term survival rates, the prognosis of patients with advanced CRC remains poor. The epithelial-mesenchymal transition (EMT) plays a pivotal role in the invasive and metastatic phenotype, which also triggers high mortality in the late stage of CRC. Furthermore, EMT also enhances the stemness features of cancers. In CRC, AT-rich interaction domain-containing protein 3B (ARID3B) has been shown as an important factor in regulating the stemness feature and immune evasion through chromatin remodeling. In this study, we aimed to investigate the role of ARID3B during the EMT process of CRC. The Cancer Genome Altas (TCGA) data indicated that both the epithelial markers (CDH1, JUP) and mesenchymal markers (FN1, VIM, Snail) were positively correlated with ARID3B, which implied ARID3B might participate in hybrid EMT. The results indicated that ectopic ARID3B expression activated EMT, and the knockdown of the ARID3B reversed EMT. Previous studies have confirmed that hypoxia would promote EMT. Interestingly, results indicated that ARID3B was activated under hypoxia-mimic conditions, including the cobalt chloride (CoCl2) treatment and 1% O2 hypoxia chamber incubation. The reporter assays also confirmed that the HIF-1α expression activated the ARID3B expression. Moreover, the knockdown of AIRD3B reversed the hypoxia-induced EMT, and the expression of ARID3B might be involved in the HIF-1α stability, which would be verified in our further experiments. Altogether, our data indicated that ARID3B was a crucial mediator for EMT and participated in the hypoxia-induced EMT in CRC. |
| 描述: | 碩士
指導教授:廖彩岑
委員:廖彩岑
委員:許銘仁
委員:李育誠 |
| 資料類型: | thesis |
| 顯示於類別: | [醫學科學研究所] 博碩士論文
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