博碩士論文 106826003 完整後設資料紀錄

DC 欄位 語言
DC.contributor系統生物與生物資訊研究所zh_TW
DC.creator黃昱齊zh_TW
DC.creatorYu Chi Huangen_US
dc.date.accessioned2019-1-21T07:39:07Z
dc.date.available2019-1-21T07:39:07Z
dc.date.issued2019
dc.identifier.urihttp://ir.lib.ncu.edu.tw:444/thesis/view_etd.asp?URN=106826003
dc.contributor.department系統生物與生物資訊研究所zh_TW
DC.description國立中央大學zh_TW
DC.descriptionNational Central Universityen_US
dc.description.abstract過去實驗室致力於探討Mitogen-Activated Protein Kinases/ Extracellular signal-Regulated Kinase (MAPK)訊息傳導路徑相關之微型核糖核酸 (miRNA)。在目前已知此訊息傳導路徑因突變而過度活化的黑色素細胞瘤 (melanoma) 中,發現諸多miRNA的過量表現 (overexpression) 均具有影響癌症相關細胞功能性能力,如增生(Proliferation)、遷移/侵襲 (Migration/Invasion)、凋亡 (Apoptosis),認為此群miRNA具有癌症抑制基因(Tumor suppressor gene)之特質,並藉由抑制黑色素細胞瘤中可能產生預後不良的風險因子以及影響諸多與癌症進展相關之重要基因,希望將來成為有潛力的標靶治療手段。zh_TW
dc.description.abstractWe dedicated to investigating Mitogen-Activated Protein Kinases/ Extracellular signal-Regulated Kinase (MAPK) pathway-associated miRNAs in our previous study. While these miRNAs are overexpressed, it could suppress the multiple functional assays related to cancer development, such as proliferation, migration, invasion, and apoptosis in melanoma which harbored the mutation(s) to make MAPK pathway active. We hope that these miRNAs play the meaningful role as tumor suppressors and they could become the promising RNA interference drug against the specific cancer.en_US
DC.subject微型核糖核酸zh_TW
DC.subject黑色素細胞瘤zh_TW
DC.subjectmiR-567en_US
DC.subjectmelanomaen_US
DC.title探討miR-567在黑色素細胞瘤中的調控機制zh_TW
dc.language.isozh-TWzh-TW
DC.titleStudy of the mechanism of miR-567 in melanomaen_US
DC.type博碩士論文zh_TW
DC.typethesisen_US
DC.publisherNational Central Universityen_US

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