miR⁃588在乳腺癌中的表达及对乳腺癌细胞增殖和侵袭的作用
作者:
作者单位:

作者简介:

通讯作者:

中图分类号:

基金项目:

宁夏人事厅留学人员资助项目;国家自然科学基金(81760482);宁夏自然科学基金(N217138);常州市科技计划资助(CE20175035)


Expression and effects of miR⁃588 on proliferation and invasion of breast cancer cells in vitro
Author:
Affiliation:

Fund Project:

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    目的:探讨miR-588在乳腺癌中的表达及对乳腺癌细胞增殖、迁移和侵袭能力的影响。方法:用化学合成的miR-588成熟模拟物(miR-588 mimic)过表达miR-588,并验证miR-588过表达率;采用MTT、克隆形成实验检测miR-588对乳腺癌细胞MCF7和MDA-MB-231增殖的影响;采用划痕愈合实验和Transwell侵袭实验检测miR-588对MDA-MB-231细胞迁移和侵袭的影响。结果:miR-588在乳腺癌组织及细胞中的相对表达均低于癌旁正常组织及乳腺正常上皮细胞;过表达miR-588能明显抑制MCF7和MDA-MB-231细胞的增殖;上调miR-588可显著抑制MDA-MB-231细胞的迁移和侵袭能力。结论:miR-588在乳腺癌中低表达,过表达miR-588可抑制乳腺癌细胞的增殖和侵袭。

    Abstract:

    Objective:This study aims to investigate the expression of miR-588 in breast cancer and its effects on proliferation,migration and invasion of breast cancer cells. Methods:The miR-588 was synthesized by chemical synthesis(miR-588 mimic),and the over expression rate of miR-588 was verified. MTT and clonogenic assay were used to detect the effect of miR-588 on the proliferation of breast cancer cells of MCF7 and MDA-MB-231. The effects of miR-588 on migration and invasion of MDA-MB-231 cells were detected by scratch healing test and Transwell invasion test. Results:MiR-588 expression in breast cancer tissues were lower than those in adjacent normal tissues and normal breast epithelial cells;Overexpression of miR-588 could inhibit proliferation of MCF7 and MDA-MB-231 cells;upregulation of miR-588 could significantly inhibit the migration and invasion of MDA-MB-231 cells. Conclusion:The expression of miR-588 is low in breast cancer. Overexpression of miR-588 can inhibit the proliferation and invasion of breast cancer cells.

    参考文献
    相似文献
    引证文献
引用本文

陶 爽,陈兴阳,程明加,徐海峰,李金平. miR⁃588在乳腺癌中的表达及对乳腺癌细胞增殖和侵袭的作用[J].南京医科大学学报(自然科学版),2019,(9):1318-1322

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2017-06-09
  • 最后修改日期:
  • 录用日期:
  • 在线发布日期: 2019-09-29
  • 出版日期:
通知关闭
郑重声明