国家神经系统疾病临床医学研究中心数据管理与共享系统

Data Management And Sharing System of China National Clinical Research Center for Neurological Diseases

Functions and Mechanisms of Tumor Necrosis Factor-alpha and Noncoding RNAs in Bone-Invasive Pituitary Adenomas

第一作者:Zhu Haibo

通讯作者:Zhang Yazhuo

基本信息

  • 负责人:Zhu Haibo
  • 数据来源: OTHERS
  • 论文编号:OTHERS20190607
  • 发表时间:2018-11-15

2018-11-15

已发表文章

发表杂志:Clinical Cancer Research

发表类型: Research Article

影响因子(IF): 12.531

PMID: 29980532 Pubmed原文链接 全文下载

主要研究背景及目的

方法

A total of 274 patients with pituitary adenomas were followed up. Transcriptomic microarrays analysis was performed on 10 pituitary adenomas, including five BIPAs and five non-bone-invasive pituitary adenomas (NBIPA). The targeted molecular markers were validated by qRT-PCR, IHC, ELISA, and osteoclast differentiation.

结论

BIPAs had worse PFS than did NBIPAs in the NGTR and NFPA groups. Inflammatory and immune factors play an important role in BIPAs. TNFa can directly induce osteoclast differentiation in BIPAs. NR_033258, lncRNA SNHG24, miR-181c-5p, and miR-454-3p can regulate TNFa expression. TNFa and its related lncRNAs and miRNAs represent potential therapeutic targets for bone-invasive pituitary adenomas in the future.

主要结果

Clinical variable analyses revealed a significant correlation between bone invasion and female sex, large tumor volume, non-gross total resection (NGTR), and tumor regrowth. BIPAs had worse progression-free survival (PFS) than did NBIPAs in the NGTR and nonfunctional pituitary adenoma (NFPA) groups. Gene ontology functional and KEGG pathway analyses showed that the biological processes and pathways were primarily immune and inflammatory pathways. Pathway act work showed that osteoclast differentiation pathway was significantly implicated in the pathway network. BIPAs had higher expression of TNFa than that of NBIPAs on IHC. In vitro, TNFa could induce RAW264.7 cells to differentiate into mature osteoclasts, leading to bone destruction. NR_033258, lncRNA SNHG24, miR-181c-5p, and miR-454-3p can regulate TNFa expression.