ASIA unversity:Item 310904400/110725
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 94286/110023 (86%)
造访人次 : 21717814      在线人数 : 318
RC Version 6.0 © 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://asiair.asia.edu.tw/ir/handle/310904400/110725


    题名: Phenethyl Isothiocyanate (PEITC) and Benzyl Isothiocyanate (BITC) Inhibit Human Melanoma A375.S2 Cell Migration and Invasion by Affecting MAPK Signaling Pathway In Vitro
    作者: MA, YI-SHIH;HS, YUNG-TING;HSIAO, YUNG-TING;LIN, JEN-JYH;CHING-LUNG, LUNG L;LIAO, CHING-LUNG;CHIN-CHUNG, L;LIN, CHIN-CHUNG
    贡献者: 生物科技學系
    日期: 2017-11
    上传时间: 2018-04-03 01:14:31 (UTC+0)
    摘要: Background/Aim: Numerous evidence has shown
    that PEITC and BITC inhibit cancer cell migration and
    invasion. In this study, we investigated the anti-metastatic
    mechanisms of PEITC and BITC in human melanoma cancer
    A375.S2 cells in vitro. Materials and Methods: We used a
    cell viability assay, an in-vitro scratch wound healing assay,
    a transwell assay for cell migration and invasion, a gelatin
    zymography assay, western blotting and EMSA to examine
    the anti-metastatic mechanisms of PEITC and BITC in
    A375.S2 cells. Results: Sublethal concentrations of PEITC
    (0, 1, 2 and 2.5 μM) and BITC (0, 0.5, 1 and 2 μM) inhibited
    mobility, migration and invasion of A375.S2 cells that were
    assayed by wound healing and Transwell filter. PEITC and
    BITC inhibited MMP-2 activity in A375.S2 cells, as assessed
    by gelatin zymography assay. Results from western blotting
    indicated that PEITC (2.5 μM) and BITC (2 μM) decreased
    the levels of p-p38 following 24 and 48 h treatment. PEITC
    (1-2.5 μM) reduced the levels of p-JNK1/2 proteins following
    48-h treatment but BITC increased p-JNK1/2 levels following
    24-h treatment. PEITC (2.5 μM) reduced the levels of pERK1/2
    proteins following 48-h treatment but BITC (0.5-2
    μM) increased p-ERK1/2 levels following 24- and 48-h
    treatment. PEITC and BITC affect cell migration and
    invasion of A375.S2 cells via MAPK pathway. PEITC and
    BITC inhibited MMP-2 activity. PEITC increased NF-ĸB
    expression but BITC decreased NF-ĸB expression in the
    nucleus. Furthermore, NF-ĸB p65 binding to DNA was
    decreased following 2.5 μM PEITC treatment, but increased
    following treatment with 1-2 μM. However, 0.5-2 μM BITC
    treatment decreased the binding of NF-ĸB to DNA in
    A375.S2 cells, as assessed by electrophoretic mobility shift
    (EMSA) assay. Conclusion: Based on these observations, we
    suggest that PEITC and BITC can be used as antimetastastic
    agents of human melanoma cells in the future.
    關聯: ANTICANCER RESEARCH
    显示于类别:[生物科技學系] 期刊論文

    文件中的档案:

    档案 大小格式浏览次数
    index.html0KbHTML408检视/开启


    在ASIAIR中所有的数据项都受到原著作权保护.


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