Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/29741
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 17524/19853 (88%)
造访人次 : 6472073      在线人数 : 682
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧:
  • 您可在西文检索词汇前后加上"双引号",以获取较精准的检索结果
  • 若欲以作者姓名搜寻,建议至进阶搜寻限定作者字段,可获得较完整数据
  • 进阶搜寻


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.cnu.edu.tw/handle/310902800/29741


    標題: Impacts of Autophagy-Inducing Ingredient of Areca Nut on Tumor Cells
    作者: Yen, Ching-Yu
    Chiang, Wei-Fan
    Liu, Shyun-Yeu
    Lin, Chung-Chih
    Liao, Kuo-An
    Lin, Che-Yi
    Hsieh, Wan-Fang
    Cheng, Yon-Chi
    Hsu, Kai-Cheng
    Lin, Pin-Yen
    Chen, Tai-Chi
    Lee, I-Ling
    Lin, Mei-Huei
    Liu, Young-Chau
    貢獻者: 生物科技系
    關鍵字: Activated protein-kinase
    Beclin1-independent autophagy
    Ampk signaling pathway
    30-100 kda fraction
    Cancer-cells
    Cross-talk
    Induction
    Apoptosis
    Macroautophagy
    aAecoline
    日期: 2015-05
    上傳時間: 2016-04-19 19:06:31 (UTC+8)
    出版者: Public Library Science
    摘要: Areca nut (AN) is a popular carcinogen used by about 0.6-1.2 billion people worldwide. Although AN contains apoptosis-inducing ingredients, we previously demonstrated that both AN extract (ANE) and its 30-100 kDa fraction (ANE 30-100K) predominantly induce autophagic cell death in both normal and malignant cells. In this study, we further explored the action mechanism of ANE 30-100K-induced autophagy (AIA) in Jurkat T lymphocytes and carcinoma cell lines including OECM-1 (mouth), CE81T/VGH (esophagus), SCC25 (tongue), and SCC-15 (tongue). The results showed that chemical-and small hairpin RNA (shRNA)-mediated inhibition of AMP-activated protein kinase (AMPK) resulted in the attenuation of AIA in Jurkat T but not in OECM-1 cells. Knockdown of Atg5 and Beclin 1 expressions ameliorated AIA in OECM-1/CE81T/VGH/Jurkat T and OECM-1/SCC25/SCC-15, respectively. Furthermore, ANE 30-100K could activate caspase-3 after inhibition of Beclin 1 expression in OECM-1/SCC25/SCC15 cells. Meanwhile, AMPK was demonstrated to be the upstream activator of the extracellular-regulated kinase (ERK) in Jurkat T cells, and inhibition of MEK attenuated AIA in Jurkat T/OECM-1/CE81T/VGH cells. Finally, we also found that multiple myeloma RPMI8226, lymphoma U937, and SCC15 cells survived from long-term non-cytotoxic ANE 30-100K treatment exhibited stronger resistance against serum deprivation through upregulated autophagy. Collectively, our studies indicate that Beclin-1 and Atg5 but not AMPK are commonly required for AIA, and MEK/ERK pathway is involved in AIA. Meanwhile, it is also suggested that long-term AN usage might increase the resistance of survived tumor cells against serum-limited conditions.
    關聯: Plos One, v.10 n.5, Article ID e0128011
    显示于类别:[生物科技系(所)] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    29741.pdf2726KbAdobe PDF174检视/开启
    index.html0KbHTML357检视/开启


    在CNU IR中所有的数据项都受到原著作权保护.

    TAIR相关文章

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈