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Title: | ELF-3 調控角質分化及侵襲在於口腔鱗狀細胞癌 ELF-3 regulates keratinocyte differentiation and invasion in oral squamous cell carcinoma |
Authors: | Mo-Fan Chang 張莫凡 |
Advisor: | 鄭永銘(Yung -MIng Jeng) |
Keyword: | 口腔鱗狀細胞癌,ELF-3,角質分化,keratin 1,NF-κB, oral squamous cell carcinoma,ELF-3,keratinocyte differentiation,keratin 1,NF-κB, |
Publication Year : | 2022 |
Degree: | 碩士 |
Abstract: | "口腔癌位居於臺灣男性十大癌症中死亡率第四位,每年將近七百人被診斷出口腔癌。口腔癌的五年存活率僅有百分之四十五。ELF-3 (E74 Like ETS Transcription Factor 3)轉錄因子是屬於上皮特異性 ETS 家族。根據之前研究, ELF-3在膀胱癌和膽管癌是抑癌基因,但在結直腸癌中是促癌基因。在這項研究中,我們發現百分之八十三的口腔鱗狀細胞癌中喪失ELF-3表達。我們發現剔除ELF-3 會增進細胞遷移。經由RNA-Seq,我們發現ELF- 3與角質分化和角質化有關。在過量表達ELF-3的SCC-25細胞中發現keratin 1和involucrin被ELF-3上調。為了解 ELF3轉錄調控機制,我們構建了 ELF-3、keratin1和involucrin螢光素酶報導基因之重組載體,並用它們在 SCC-25細胞中進行螢光素酶的活性實驗,我們證實了 ELF-3 上調會促進keratin 1上升。而經TPA (12-O-tetradecanoylphorbol-13-acetate) 和鈣處理過的 SCC-25 會使得ELF-3上升。此外我們使用PathDetct 系統發現 ELF-3誘導了 NF-κB 報導基因的活性,西方墨點法證實NF-κB 的p65次單位的磷酸化也為之增強,證實ELF-3 可活化 NF-κB途徑。總之,我們的結論指出ELF-3 是口腔鱗狀細胞癌的抑癌基因,可抑制腫瘤遷移和促進分化。活化NF-κB的路徑可能是ELF-3增加角質分化的機制。" |
URI: | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/82879 |
DOI: | 10.6342/NTU202200077 |
Fulltext Rights: | 未授權 |
metadata.dc.date.embargo-lift: | 2025-01-13 |
Appears in Collections: | 病理學科所 |
Files in This Item:
File | Size | Format | |
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U0001-1601202222292000.pdf Restricted Access | 1.87 MB | Adobe PDF |
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