首页> 美国卫生研究院文献>Journal of Cellular and Molecular Medicine >MiR‐34b‐3p represses cell proliferation cell cycle progression and cell apoptosis in non‐small‐cell lung cancer (NSCLC) by targeting CDK4
【2h】

MiR‐34b‐3p represses cell proliferation cell cycle progression and cell apoptosis in non‐small‐cell lung cancer (NSCLC) by targeting CDK4

机译:MiR-34b-3p通过靶向CDK4抑制非小细胞肺癌(NSCLC)中的细胞增殖细胞周期进程和细胞凋亡

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Lung cancer is the most common incident cancer, with a high mortality worldwide, and non‐small‐cell lung cancer (NSCLC) accounts for approximately 85% of cases. Numerous studies have shown that the aberrant expression of microRNAs (miRNAs) is associated with the development and progression of cancers. However, the clinical significance and biological roles of most miRNAs in NSCLC remain elusive. In this study, we identified a novel miRNA, miR‐34b‐3p, that suppressed NSCLC cell growth and investigated the underlying mechanism. miR‐34b‐3p was down‐regulated in both NSCLC tumour tissues and lung cancer cell lines (H1299 and A549). The overexpression of miR‐34b‐3p suppressed lung cancer cell (H1299 and A549) growth, including proliferation inhibition, cell cycle arrest and increased apoptosis. Furthermore, luciferase reporter assays confirmed that miR‐34b‐3p could bind to the cyclin‐dependent kinase 4 (CDK4) mRNA 3′‐untranslated region (3′‐UTR) to suppress the expression of CDK4 in NSCLC cells. H1299 and A549 cell proliferation inhibition is mediated by cell cycle arrest and apoptosis with CDK4 interference. Moreover, CDK4 overexpression effectively reversed miR‐34‐3p‐repressed NSCLC cell growth. In conclusion, our findings reveal that miR‐34b‐3p might function as a tumour suppressor in NSCLC by targeting CDK4 and that miR‐34b‐3p may, therefore, serve as a biomarker for the diagnosis and treatment of NSCLC.
机译:肺癌是最常见的事件性癌症,在世界范围内死亡率很高,非小细胞肺癌(NSCLC)约占病例的85%。大量研究表明,microRNA(miRNA)的异常表达与癌症的发生和发展有关。但是,大多数miRNA在NSCLC中的临床意义和生物学作用仍然难以捉摸。在这项研究中,我们鉴定了一种抑制NSCLC细胞生长的新型miRNA miR-34b-3p,并研究了其潜在机制。 NSCLC肿瘤组织和肺癌细胞系(H1299和A549)中的miR-34b-3p均下调。 miR-34b-3p的过表达抑制了肺癌细胞(H1299和A549)的生长,包括增殖抑制,细胞周期阻滞和凋亡增加。此外,萤光素酶报告基因测定证实,miR-34b-3p可以与细胞周期蛋白依赖性激酶4(CDK4)mRNA 3'-非翻译区(3'-UTR)结合,从而抑制CDK4在NSCLC细胞中的表达。 H1299和A549细胞增殖抑制作用是由CDK4干扰引起的细胞周期停滞和凋亡介导的。此外,CDK4过表达有效地逆转了miR-34-3p抑制的NSCLC细胞的生长。总之,我们的发现表明,miR-34b-3p可能通过靶向CDK4发挥NSCLC的抑癌作用,因此miR-34b-3p可以作为NSCLC诊断和治疗的生物标志物。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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