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    Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/34521


    標題: A novel mechanism driving poor-prognostic gastric cancer: overexpression of the transcription factor Kruppel-like factor 16 promotes growth and metastasis of gastric cancer through regulating the Notch pathway
    作者: Sun, Ding-Ping
    Tian, Yu-Feng
    Lin, Chih-Chan
    Hung, Shih-Ting
    Uen, Yih-Huei
    Hseu, You-Cheng
    Chou, Chia-Lin
    Cheng, Li-Chin
    Wang, Wen-Ching
    Kuang, Yi-Yu
    Fang, Chia-Lang
    Lin, Kai-Yuan
    貢獻者: Chi Mei Med Ctr, Dept Surg
    Chia Nan Univ Pharm & Sci, Dept Food Sci & Technol
    Chi Mei Med Ctr, Dept Med Res
    Asia Univ Hosp, Dept Surg
    Asia Univ, Dept Biotechnol
    Tainan Municipal Nan Hosp, Dept Surg
    China Med Univ, Dept Cosmeceut
    Asia Univ, Dept Hlth & Nutr Biotechnol
    China Med Univ, Chinese Med Res Ctr
    Taipei Med Univ, Sch Med, Coll Med, Dept Pathol
    Taipei Med Univ Hosp, Taipei Med Univ, Dept Pathol
    Chia Nan Univ Pharm & Sci, Dept Biotechnol
    關鍵字: Gastric cancer
    KLF16
    prognosis
    MFAP5
    Notch pathway
    日期: 2021
    上傳時間: 2023-11-11 12:00:45 (UTC+8)
    出版者: E-CENTURY PUBLISHING CORP
    摘要: Gastric cancer (GC) is one of the most common malignant tumors worldwide and has high rates of morbidity and mortality. This study investigated the role of Kruppel-like factor 16 (KLF16) in GC. Real-time polymerase chain reaction, Western blotting, and immunohistochemistry were used to examine the expression of KLF16 in gastric cells and tissues. Gene overexpression and silencing were applied to study the involvement of KLF16 in GC cell growth and metastasis along with its underlying mechanism. The results indicate that KLF16 overexpression is significantly associated with nodal status, distant metastasis, staging, degree of differentiation, vascular invasion, and patient survival. Multivariate Cox proportional hazards regression model analysis revealed that the overexpression of KLF16 is an independent prognostic biomarker of GC. The in vitro study revealed that up-regulated KLF16 accelerates cell growth and metastasis, whereas the inhibition of KLF16 suppresses these cellular activities. The results of an animal study also indicated that the overexpression and silencing of KLF16 accelerate and repress xenograft proliferation and metastasis. Further studies of affected cell growth and metastasis revealed that KLF16 modulates the cell cycle and epithelial-mesenchymal transition through transcriptional regulation of microfibrillar-associated protein 5. Collectively, these results reveal that KLF16 overexpression is a potential prognostic biomarker and therapeutic target for the treatment of GC.
    關聯: AM J CANCER RES, v.11, n.6, pp.2717-2735
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