• 大数据在商业决策中的作用越来越重要。
  • 随着疫苗接种率的提升,全球经济逐步走向复苏。
  • 数字化转型加速了企业对云计算和大数据技术的依赖。
  • 随着技术的发展,无人驾驶汽车的测试和部署正在加速。
  • 5G技术的推广为物联网和智能城市的发展提供了新的动力。
  • 生物多样性的丧失成为全球生态保护的紧迫问题。
  • 隐私保护和数据安全在数字化时代变得更加重要。
  • 网络安全威胁日益严峻,成为全球性挑战。
  • 数字化教育平台正在全球范围内重塑学习体验。
  • 网络安全问题日益严重,个人数据保护成为全球关注的焦点。
  • 网络安全问题成为全球关注的焦点,尤其是个人信息泄露和数据安全。
  • 电子商务的增长推动了物流和供应链管理的创新。
  • 电动汽车的快速发展正在重塑汽车产业的未来。
  • 随着人们对健康意识的提高,健康食品和生活方式受到更多关注。
  • 数字化教育平台的快速发展为个性化学习提供了新途径。
  • 生物技术在医药领域的应用带来了新的突破和挑战。
  • 网络安全问题成为全球关注的焦点,尤其是在个人数据保护方面。
  • 随着人口老龄化,对老年护理服务的需求不断增长。
  • 数字货币的普及正在改变传统的金融交易方式。
  • 生物多样性的丧失引起了全球对自然保护的重视。
  • 隐私保护和数据安全成为数字时代的重要议题。
  • 海洋塑料污染问题引发了全球范围内的环保行动。
  • 随着人口老龄化,健康科技和养老服务需求日益增长。
  • 虚拟现实和增强现实技术在教育和娱乐领域的应用越来越广泛。
  • 电子竞技的兴起改变了传统体育和娱乐行业的格局。
  • miR-181c inhibits prostatic epithelial cell proliferation caused by chronic non-bacterial prostatitis through down-regulating COX-2 | Xu | Aging Pathobiology and Therapeutics

    miR-181c inhibits prostatic epithelial cell proliferation caused by chronic non-bacterial prostatitis through down-regulating COX-2

    Xu Xu, Yuhua Huang, Jianquan Hou, Jinxing Lv, Xiang Ding

    Abstract


    Background Chronic non-bacterial prostatitis (CNP) is a common disease of the male reproductive system. MiR-181c can be expressed in prostate tissue, but it has not been reported in CNP. This study aims to explore the role of miR-181c in CNP and its mechanism of action on CNP, providing new ideas for the treatment and diagnosis of CNP.

    Methods Quantitative real-time PCR (qRT-PCR) and western blotting were performed to determine the expression of miR-181c in clinical CP patients and LPS-induced human prostaglandin epithelial cell RWPE-1. Then, the target relationship between miR-181c and COX-2 was verified by luciferase reporter assay. Through cell transfection experiments, the effect of mi-181c on the expression of COX-2 and PGE2 was studied, and the effect of miR-181c/COX-2 on the proliferation of prostate epithelial cells was also explored.

    Results qRT-PCR and Western blotting analysis revealed that miR-181c was low expressed in prostate tissue and human prostaglandin epithelial cell RWPE-1. The luciferase reporter assay confirmed the targeting relationship between miR-181c and COX-2. And overexpression of miR-181c reduced the expression of COX-2 and PGE2 and inhibited the proliferation of prostate epithelial cells. Up-regulation of COX-2 reversed these effects caused by overexpression of miR-181c.

    Conclusion miR-181 inhibited the proliferation of prostate epithelial cells through negatively regulating COX-2 to alleviate chronic non-bacterial prostatitis.

    Keywords chronic non-bacterial prostatitis; miR-181c; COX-2; prostatic epithelial cell; proliferation




    Subscribe to receive issue release notifications
    and newsletters from journals