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    標題: Long Non-Coding RNA MIR31HG Promotes the Transforming Growth Factor β-Induced Epithelial-Mesenchymal Transition in Pancreatic Ductal Adenocarcinoma Cells
    作者: Ko, Ching-Chung
    Hsieh, Yao-Yu
    Yang, Pei-Ming
    貢獻者: Chi Mei Hospital
    Chia Nan University of Pharmacy & Science
    National Sun Yat Sen University
    Taipei Medical University
    Shuang Ho Hospital
    Taipei Medical University
    Taipei Medical University
    Taipei Medical University
    Academia Sinica - Taiwan
    Taipei Medical University
    Taipei Medical University
    Taipei Municipal WanFang Hospital
    Taipei Medical University
    Taipei Medical University
    關鍵字: cancer cells
    lncrna mir31hg
    breast-cancer
    expression
    proliferation
    prognosis
    migration
    invasion
    日期: 2022
    上傳時間: 2023-12-11 14:00:32 (UTC+8)
    出版者: MDPI
    摘要: The epithelial-to-mesenchymal transition (EMT) describes a biological process in which polarized epithelial cells are converted into highly motile mesenchymal cells. It promotes cancer cell dissemination, allowing them to form distal metastases, and also involves drug resistance in metastatic cancers. Transforming growth factor beta (TGF beta) is a multifunctional cytokine that plays essential roles in development and carcinogenesis. It is a major inducer of the EMT. The MIR31 host gene (MIR31HG) is a newly identified long non-coding (lnc)RNA that exhibits ambiguous roles in cancer. In this study, a cancer genomics analysis predicted that MIR31HG overexpression was positively correlated with poorer disease-free survival of pancreatic ductal adenocarcinoma (PDAC) patients, which was associated with upregulation of genes related to TGF beta signaling and the EMT. In vitro evidence demonstrated that TGF beta induced MIR31HG expression in PDAC cells, and knockdown of MIR31HG expression reversed TGF beta-induced EMT phenotypes and cancer cell migration. Therefore, MIR31HG has an oncogenic role in PDAC by promoting the EMT.
    關聯: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.23, n.CB2, pp.CC2, pp.-762, SI
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