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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31003


    標題: Role of galectin-1 in urinary bladder urothelial carcinoma cell invasion through the JNK pathway
    作者: Shen, Kun-Hung
    Li, Chien-Feng
    Chien, Lan-Hsiang
    Huang, Cheng-Hao
    Su, Chia-Cheng
    Liao, Alex C.
    Wu, Ting-Feng
    貢獻者: Southern Taiwan Univ Sci & Technol, Dept Biotechnol
    Chi Mei Med Ctr, Dept Urol
    Taipei Med Univ, Dept Urol
    Chi Mei Med Ctr, Dept Pathol
    Natl Sun Yat Sen Univ, Inst Biomed Sci
    Natl Hlth Res Inst, Natl Inst Canc Res
    Nan Pao Resins Chem Co Ltd
    Chia Nan Univ Pharm & Sci, Dept Senior Citizen Serv Management
    Southern Taiwan Univ Sci & Technol, Ctr Gen Educ
    關鍵字: Galectin-1
    invasion
    JNK
    shRNA
    urothelial bladder urinary carcinoma
    日期: 2016-10
    上傳時間: 2018-01-18 11:39:37 (UTC+8)
    出版者: Wiley-Blackwell
    摘要: Human galectin-1 is a member of the galectin family, proteins with conserved carbohydrate-recognition domains that bind galactoside. Galectin-1 is highly expressed in various tumors and participates in various oncogenic processes. However, detailed descriptions of the function of galectin-1 in urinary bladder urothelial carcinoma have not been reported. Our previous cohort investigation showed that galectin-1 is associated with tumor invasiveness and is a possible independent prognostic marker of urinary bladder urothelial carcinoma. The present study aimed to clarify the relevance of galectin-1 expression level to tumor progression and invasion. In order to decipher a mechanism for the contribution of galectin-1 to the malignant behavior of urinary bladder urothelial carcinoma, two bladder cancer cell lines (T24 and J82) were established with knockdown of galectin-1 expression by shRNA. Bladder cancer cells with LGALS1 gene silencing showed reduced cell proliferation, lower invasive capability, and lower clonogenicity. Extensive signaling pathway studies indicated that galectin-1 participated in bladder cancer cell invasion by mediating the activity of MMP9 through the Ras-Rac1-MEKK4-JNK-AP1 signaling pathway. Our functional analyses of galectin-1 in urinary bladder urothelial carcinoma provided novel insights into the critical role of galectin-1 in tumor progression and invasion. These results revealed that silencing the galectin-1-mediated MAPK signaling pathway presented a novel strategy for bladder cancer therapy.
    關聯: Cancer Science, v.107 n.10, pp.1390-1398
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