...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of cellular physiology. >LncRNA SNHG3 is activated by E2F1 and promotes proliferation and migration of non-small-cell lung cancer cells through activating TGF-β pathway and IL-6/JAK2/STAT3 pathway
【24h】

LncRNA SNHG3 is activated by E2F1 and promotes proliferation and migration of non-small-cell lung cancer cells through activating TGF-β pathway and IL-6/JAK2/STAT3 pathway

机译：LncRNA SNHG3 E2F1激活和促进非小细胞的增殖和迁移肺癌细胞通过激活TGF -β途径和il - 6 / JAK2 / STAT3通路

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

Recently, long noncoding RNAs (IncRNAs) have been widely reported to play pivotal roles in the regulation of human cancers. Although the oncogenic property of IncRNA small nucleolar RNA host gene 3 (SNHG3) has been revealed in a variety of cancers, functions and regulatory mechanism of SNHG3 in non-small-cell lung cancer (NSCLC) remain to be investigated. In this study, we detected the upregulated expression of SNHG3 in NSCLC tissues as well as cells through quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis. Using Kaplan-Meier analysis, we determined that a high-level of SNHG3 was associated with a low overall survival rate of patients with NSCLC. Through gain and loss of function experiments, we demonstrated that SNHG3 had a significantly positive effect on NSCLC cell proliferation and migration. Mechanistic investigations revealed that SNHG3 was a predicted direct transcriptional target of E2F1. We observed that the transcriptional activation of SNHG3 could be induced by E2F1. To explore the mechanism, rescue experiments were carried out, which revealed that the cotreatment with SB-431542, JSI-124, or JSI-124 + SB-431542 rescued the effects brought by the overexpression of SNHG3 on NSCLC cell proliferation, migration, and epithelial-mesenchymal transition process. Our results suggested that E2F1 activated SNHG3 and promoted cell proliferation and migration in NSCLC via transforming growth factor-β pathway and interleukin-6/janus-activated kinase 2/signal transducer and activator of transcription 3 pathway, which implied that SNHG3 may be a biomarker for the treatment of patients with NSCLC.
机译：最近,长非编码rna (IncRNAs)广泛报道中扮演关键角色监管的人类癌症。致癌的属性IncRNA小核仁的RNA宿主基因3 (SNHG3)被发现在一个各种各样的癌症,功能和监管在非小细胞肺癌SNHG3机制(NSCLC)仍有待调查。我们发现调节SNHG3的表情在非小细胞肺癌组织和细胞定量逆转录聚合酶连锁反应(存在)的分析。kaplan meier分析,我们确定一个高层的SNHG3较低有关与非小细胞肺癌患者的总体生存率。通过功能实验的得失,我们证明SNHG3显著对非小细胞肺癌细胞增殖和积极的影响迁移。SNHG3是预测直接转录E2F1的目标。转录激活SNHG3E2F1引起的。实验进行了显示与某人cotreatment - 431542, - 124, jsi或jsi - 124 - 431542 +某人救了带来的影响SNHG3在非小细胞肺癌细胞的过度增殖、迁移和epithelial-mesenchymal过渡过程。结果表明,E2F1 SNHG3和激活促进细胞增殖和迁移非小细胞肺癌通过转化生长因子-β通路和白细胞介素- 6 / janus-activated激酶2 /信号传感器和转录激活3暗示SNHG3可能途径生物治疗的患者非小细胞肺癌。

著录项

相似文献

  • 外文文献
  • 中文文献
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