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DBX2 Promotes Glioblastoma Cell Proliferation by Regulating REST Expression.
Current Pharmaceutical Biotechnology ( IF 2.2 ) Pub Date : 2022-01-01 , DOI: 10.2174/1389201022666210830142827
Ruixing He 1 , Xiaotian Zhang 2 , Lianshu Ding 1
Affiliation  

BACKGROUND Glioblastoma (GBM) is the most common but lethal brain cancer with poor prognosis. The developing brain homeobox 2 (DBX2) has been reported to play important roles in tumor growth. However, the mechanisms of DBX2 in GBM are still unknown. OBJECTIVES This study aims to investigate the function and mechanisms of DBX2 in GBM. METHODS The expressions of DBX2 and REST in GBM were measured by analyzing data from databases, and the results were checked by qPCR and/or western blot of GBM cell lines. Cell proliferation was determined by CCK8 assay, immunohistochemistry and colony formation assay. ChIP-qPCR was used to determine the binding sites of DBX2 on REST. RESULTS In this study, we found that the expression of DBX2 was upregulated in the GBM cell lines. The cell proliferation was damaged after blocking DBX2 expression in U87 and U251 GBM cell lines. The expression level of DBX2 had a positive relationship with that of REST. Our ChIPqPCR results showed that DBX2 is directly bound to the promoter region of REST. Additionally, the increased GBM cell proliferation caused by DBX2 overexpression can be rescued by REST loss of function. CONCLUSION DBX2 could promote cell proliferation of GBM by binding to the promoter region of REST gene and increasing REST expression.

中文翻译:

DBX2 通过调节 REST 表达促进胶质母细胞瘤细胞增殖。

背景 胶质母细胞瘤 (GBM) 是最常见但致命的脑癌,预后较差。据报道,发育中的大脑同源框 2 (DBX2) 在肿瘤生长中起重要作用。然而,GBM 中 DBX2 的机制仍然未知。目的 本研究旨在探讨 DBX2 在 GBM 中的功能和机制。方法通过分析数据库中的数据,测量GBM中DBX2和REST的表达,并通过qPCR和/或GBM细胞系的蛋白质印迹检查结果。通过CCK8测定、免疫组织化学和集落形成测定确定细胞增殖。ChIP-qPCR 用于确定 DBX2 在 REST 上的结合位点。结果在本研究中,我们发现GBM细胞系中DBX2的表达上调。在 U87 和 U251 GBM 细胞系中阻断 DBX2 表达后,细胞增殖受到损害。DBX2的表达水平与REST的表达水平呈正相关。我们的 ChIPqPCR 结果显示 DBX2 直接与 REST 的启动子区域结合。此外,由 DBX2 过表达引起的 GBM 细胞增殖增加可以通过 REST 功能丧失来挽救。结论 DBX2通过与REST基因启动子区结合,增加REST表达,促进GBM细胞增殖。
更新日期:2021-08-30
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