...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Inhibition of proliferation, invasion and adhesion of liver cancer cells by 5-azacytidine and butyrate.
【24h】

Inhibition of proliferation, invasion and adhesion of liver cancer cells by 5-azacytidine and butyrate.

机译：5-氮杂胞苷和丁酸盐抑制肝癌细胞的增殖，侵袭和粘附。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

BACKGROUND: The prognosis for liver cancer is poor with current chemotherapeutic agents, for the most part, ineffective. We have recently shown that 5-azacytidine (5-azaC) and butyrate stimulate apoptosis in two human liver cancer cell lines (HepG2 and Hep3B). The purpose of our present study was to determine the effects of these agents on proliferation, invasion and adhesion of liver cancer cells, and to assess potential cellular mechanisms for these effects. MATERIALS AND METHODS: HepG2 and Hep3B cells were treated with either 5-azaC (8 microM), sodium butyrate (35 mM), 5-azaC + butyrate or vehicle (control); proliferation, cellular invasion and adherence were determined. Western blots were performed to assess expression levels of p21waf1, p27kip1 and p53. RESULTS: Treatment with 5-azaC alone inhibited invasion of Hep3B cells whereas butyrate alone inhibited invasion of HepG2 cells; the combination of 5-azaC + butyrate completely suppressed the invasion of both cell lines. Moreover, cellular adhesion and proliferation were inhibited in both cell lines by combination treatment. Levels of the Cdk inhibitor p21waf1 were increased in HepG2 cells after 5-azaC and in both cell lines after butyrate treatment; levels of p27kip1 were increased in both cell lines after either 5-azaC or butyrate treatment. CONCLUSIONS: Our results demonstrate that the combination of 5-azaC and butyrate effectively blocks proliferation, invasion and cellular adhesion of both HepG2 and Hep3B cells. Increases in the expression of the cell cycle inhibitory proteins, p21waf1 and p27kip1 suggest that these effects may be mediated through the induction of these inhibitory proteins. Agents such as 5-azaC and butyrate that target the cell cycle pathway may prove clinically useful in the adjuvant treatment of liver cancers.
机译：背景：目前的化疗药物对肝癌的预后很差，大多数情况下无效。我们最近显示，5-氮杂胞苷（5-azaC）和丁酸盐刺激两种人肝癌细胞系（HepG2和Hep3B）的凋亡。我们本研究的目的是确定这些药物对肝癌细胞增殖，侵袭和粘附的影响，并评估这些作用的潜在细胞机制。材料与方法：用5-azaC（8 microM），丁酸钠（35 mM），5-azaC +丁酸钠或赋形剂（对照）处理HepG2和Hep3B细胞。确定增殖，细胞侵袭和粘附。进行了蛋白质印迹以评估p21waf1，p27kip1和p53的表达水平。结果：单独用5-azaC处理可抑制Hep3B细胞的侵袭，而单独使用丁酸酯可抑制HepG2细胞的侵袭。 5-氮杂碳+丁酸酯的组合完全抑制了两种细胞系的侵袭。此外，通过联合处理在两种细胞系中均抑制了细胞粘附和增殖。在5-azaC处理后的HepG2细胞和丁酸处理后的两种细胞系中，Cdk抑制剂p21waf1的水平均升高; 5-azaC或丁酸盐处理后，两种细胞系中p27kip1的水平均升高。结论：我们的结果表明5-氮杂碳和丁酸酯的组合有效地阻止了HepG2和Hep3B细胞的增殖，侵袭和细胞粘附。细胞周期抑制蛋白p21waf1和p27kip1表达的增加表明，这些作用可能是通过诱导这些抑制蛋白来介导的。靶向细胞周期途径的药物如5-azaC和丁酸盐可能在临床上可用于肝癌的辅助治疗。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号