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    ASIA unversity > 管理學院 > 經營管理學系  > 期刊論文 >  Item 310904400/81198

    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/81198

    Title: Osthole inhibits insulin-like growth factor-1-induced epithelial to mesenchymal transition via the inhibition of PI3K/Akt signaling pathway in human brain cancer cells
    Authors: Ying-Chao Lin;Jia-Ching Lin;Chao-Ming Hung;Yeh Chen;Liang-Chih Liu;Tin-Chang Chang;Jung-Yie Kao;Chi-Tang Ho;Tzong-Der Way
    Contributors: 經營管理學系
    Date: 2014-05
    Issue Date: 2014-10-01 16:51:41 (UTC+8)
    Abstract: lioblastoma multiforme (GBM) is one of the most lethal types of tumors and highly metastatic and invasive. The epithelial-to-mesenchymal transition (EMT) is the crucial step for cancer cells to initiate the metastasis and could be induced by many growth factors. In this study, we found that GBM8401 cells were converted to fibroblastic phenotype and the space between the cells became expanded in response to insulin-like growth factor-1 (IGF-1) treatment. Epithelial markers were downregulated and mesenchymal markers were upregulated simultaneously after IGF-1 treatment. Our results illustrate that IGF-1 was able to induce EMT in GBM8401 cells. Osthole would reverse IGF-1-induced morphological changes, upregulated the expression of epithelial markers, and downregulated the expression of mesenchymal markers. Moreover, wound-healing assay also showed that osthole could inhibit IGF-1-induced migration of GBM8401 cells. By using dual-luciferase reporter assay and real-time PCR, we demonstrated that osthole inhibited IGF-1-induced EMT at the transcriptional level. Our study found that osthole decreased the phosphorylation of Akt and GSK3β and recovered the GSK3β bioactivity in inhibiting EMT transcription factor Snail and Twist expression. These results showed that osthole inhibited IGF-1-induced EMT by blocking PI3K/Akt pathway. We hope that osthole can be used in anticancer therapy and be a new therapeutic medicine for GBM in the future.
    Appears in Collections:[經營管理學系 ] 期刊論文

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