• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Anti-cancer drugs >MiR-29a inhibits cell proliferation and migration by targeting the CDC42/PAK1 signaling pathway in cervical cancer
【24h】

MiR-29a inhibits cell proliferation and migration by targeting the CDC42/PAK1 signaling pathway in cervical cancer

机译：MiR-29A通过靶向宫颈癌中的CDC42 / PAK1信号通路来抑制细胞增殖和迁移

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

Cervical cancer is the second most common gynecological malignancy worldwide and the tumorigenesis mechanisms of cervical cancer are still unclear. This study aimed to reveal the role of miR-29a in cervical cancer. The expression level of miR-29a and CDC42 was measured using qRT-PCR. Cell proliferation, apoptosis, migration, and invasion were detected using colony formation, flow cytometry analysis, wound-healing assay, and Transwell assay, respectively. Luciferase reporter assay was used to determine the binding of miR-29a with CDC42. CDC42/p21-activated kinase 1 (PAK1) pathway-related proteins were measured by western blotting. MiR-29a was downregulated and CDC42 was upregulated in cervical cancer cells. Luciferase reporter assay showed that miR-29a negatively regulated the expression of CDC42 by directly targeting 3 '-UTR of CDC42. Cell proliferation, migration, and invasion were markedly inhibited, whereas cell apoptosis was significantly increased in Hela and CaSki cells transfected with miR-29a mimics. These effects were partly recovered by CDC42 overexpression. Protein levels of PAK1, p-PAK1, p-LIMK, and p-cofilin were significantly downregulated by miR-29a mimics, which was reversed by CDC42 overexpression and was increased by the miR-29a inhibitor. MiR-29a inhibited cell proliferation, migration, and invasion, as well as promoted cell apoptosis through repressing the PAK1/LIMK signaling pathway by targeting CDC42 in cervical cancer.
机译：宫颈癌是全球第二个最常见的妇科恶性肿瘤，宫颈癌的肿瘤发生机制仍然不清楚。本研究旨在揭示miR-29a在宫颈癌中的作用。使用QRT-PCR测量miR-29a和cdc42的表达水平。使用菌落形成，流式细胞术分析，伤口愈合测定和Transwell测定分别检测细胞增殖，细胞凋亡，迁移和侵袭。荧光素酶报告器测定用于确定miR-29a与cdc42的结合。通过蛋白质印迹测量CDC42 / P21活性激酶1（PAK1）途径相关蛋白。下调miR-29a，CDC42在宫颈癌细胞中上调。荧光素酶报告结果显示，MiR-29A通过直接靶向CDC42的3'-FUTR来负调节CDC42的表达。细胞增殖，迁移和侵袭显着抑制，而MIR-29A模拟中的Hela和Caski细胞中细胞凋亡显着增加。 CDC42过表达部分回收这些效果。 MiR-29A模拟物显着下调PAK1，P-P-PAK1，P-LIMK和P-COFILIN的蛋白质水平，其通过CDC42过表达逆转，并通过MIR-29A抑制剂增加。 miR-29a通过靶向CDC42在宫颈癌中诱导PAK1 / LIMK信号通路，抑制细胞增殖，迁移和侵袭，以及促进细胞凋亡。

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