...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell cycle >Overexpression of lncRNA GAS5 suppresses prostatic epithelial cell proliferation by regulating COX-2 in chronic non-bacterial prostatitis
【24h】

Overexpression of lncRNA GAS5 suppresses prostatic epithelial cell proliferation by regulating COX-2 in chronic non-bacterial prostatitis

机译：LNCRNA气体的过度表达通过调节慢性非细菌前列腺炎中的COX-2来抑制前列腺上皮细胞增殖

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

Chronic non-bacterial prostatitis (CNP) is a common urologic disease that is linked to the development of prostate cancer. Long non-coding RNA (lncRNA) GAS5 has been identified to mediate cell proliferation in prostate cancer, although its role in CNP is still unclear. Human prostate epithelial cell line RWPE-1 was induced by lipopolysaccharide (LPS) to mimic CNP model in vitro. Real-time PCR was performed to determine the expression of GAS5 and COX-2, while western blotting was used to evaluate the protein expression of COX-2. The interaction between GAS5 and COX-2 was determined using RNA pull-down and RNA immunoprecipitation (RIP). Cell proliferation was determined using MTT assay. The expression of GAS5 was decreased, while COX-2 was increased in prostatitis tissues and in LPS-induced RWPE-1 cells. The overexpression of GAS5 suppressed the protein level of COX-2, and inhibited cell proliferation of LPS-induced RWPE-1 cells and HPECs, which was rescued by the co-transfection with pcDNA-GAS5 and pcDNA-COX-2. GAS5 was confirmed to promote the ubiquitination of COX-2, and the in vivo GAS5-overexpressed CNP rat model decreased the motor scores, the volume of prostate tissues, the average number of inflammatory cells, prostatic proliferation, and COX-2 expression. Our findings revealed that overexpression of GAS5 inhibited cell proliferation via negatively regulating the expression of COX-2, thus alleviating the progression of CNP.
机译：慢性非细菌前列腺炎（CNP）是一种常见的泌尿病疾病，与前列腺癌的发育有关。已经鉴定了长的非编码RNA（LNCRNA）Gas5以介导前列腺癌中的细胞增殖，尽管其在CNP中的作用尚不清楚。通过脂多糖（LPS）诱导人前列腺上皮细胞系RWPE-1以体外模拟CNP模型。进行实时PCR以确定气体5和COX-2的表达，而Western印迹用于评估COX-2的蛋白质表达。使用RNA下拉和RNA免疫沉淀（RNA免疫沉淀（RNA）测定气体5和COX-2之间的相互作用。使用MTT测定法测定细胞增殖。气体5的表达降低，而COX-2在前列腺炎组织和LPS诱导的RWPE-1细胞中增加。气体5的过表达抑制了COX-2的蛋白质水平，并抑制了LPS诱导的RWPE-1细胞和HPEC的细胞增殖，其被PCDNA - 气体5和PCDNA-COX-2的共转染抵抗。确认Gas5促进COX-2的泛素，并且体内气体5-过表达的CNP大鼠模型降低了电动机分数，前列腺组织的体积，炎性细胞的平均数，前列腺增殖和COX-2表达。我们的研究结果显示，通过对COX-2的表达产生负面调节CNP的进展，通过对抗抑制细胞增殖抑制细胞增殖。

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