ASIA unversity:Item 310904400/108068
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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/108068


    Title: MicroRNA-200c inhibits epithelial-mesenchymal transition, invasion, and migration of lung cancer by targeting HMGB1
    Authors: Po-Len Liu;Wei-Lun Liu;Jia-Ming Cha;Jia-Ming Chang;陳永祥;Yung-Hsian Chen;Yu-Peng Liu;Hsuan-Fu Kuo;Chong-Chao H;Chong-Chao Hsieh;Yu-Sian Ding;Wei-Wei Chen;Inn-Wen Chon;Inn-Wen Chong
    Contributors: 心理學系
    Date: 2017-07
    Issue Date: 2017-10-27 16:45:35 (UTC+8)
    Abstract: MicroRNAs (miRs) play critical roles in cancer development, proliferation, epithelial-mesenchymal transition (EMT), invasion, and migration through regulating the expression of oncogenes and tumour suppressor genes. Previous studies have indicated that miR-200c acts as a tumour suppressor in various cancers by downregulating high-mobility group box 1 (HMGB1) and thereby suppressing EMT and metastasis. In addition, miR-200c was reported to be downregulated and correlated with poor outcomes in non-small cell lung cancer (NSCLC). However, its functional role in HMGB1 regulation in NSCLC is still unclear. This study aimed to clarify whether miR-200c acts as a tumour suppressor in NSCLC by downregulating HMGB1, which is associated with EMT, invasion, cytoskeleton rearrangement, and migration in vitro and in vivo. In order to demonstrate HMGB1 downregulation by miR-200c, the NSCLC cell line A549 was transfected with miR-200c mimic or inhibitor. The mimic significantly reduced HMGB1 expression and suppressed EMT, invasion, and migration, while the inhibitor generated the opposite effects. Additionally, using xenograft mouse models, we confirmed that HMGB1 overexpression increased tumour EMT. In summary, our results demonstrated that miR-200c could suppress EMT, invasion, and migration of NSCLC cells by downregulating HMGB1.
    Relation: PLoS One.
    Appears in Collections:[Department of Psychology] Journal Article

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