Suppr超能文献

叉头框蛋白D1的沉默抑制胶质瘤细胞的增殖和迁移。

Silencing of Forkhead box D1 inhibits proliferation and migration in glioma cells.

作者信息

Gao Yuan-Feng, Zhu Tao, Mao Xiao-Yuan, Mao Chen-Xue, Li Ling, Yin Ji-Ye, Zhou Hong-Hao, Liu Zhao-Qian

机构信息

Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

出版信息

Oncol Rep. 2017 Feb;37(2):1196-1202. doi: 10.3892/or.2017.5344. Epub 2017 Jan 2.

Abstract

Despite the extensive role of Forkhead box transcription factors in the development and progression of various cancers, little is known about their role in glioma. We examined the expression and function of Forkhead box D1 (FOXD1) in glioma cell behavior and found that FOXD1 was upregulated and directly correlated with the glioma grade. Data analysis also revealed significant differences in FOXD1 expression for both gene expression profiles (GSE4290 and GSE7696) and the TCGA datasets. Additionally, decreased FOXD1 expression in U251 and U87 glioma cells caused a delay in cell growth and a disruption in colony formation. FOXD1 silencing also promoted generation of apoptotic bodies containing nuclear fragments. Cells with suppressed expression of FOXD1 markedly reduced glioma cell migration. Our results suggest that FOXD1 may serve as a novel regulator of glioblastoma cell behavior that may offer a novel target for gene targeted glioma therapies.

摘要

尽管叉头框转录因子在多种癌症的发生和发展中发挥着广泛作用,但它们在胶质瘤中的作用却鲜为人知。我们研究了叉头框D1(FOXD1)在胶质瘤细胞行为中的表达和功能,发现FOXD1表达上调且与胶质瘤分级直接相关。数据分析还显示,在基因表达谱(GSE4290和GSE7696)以及TCGA数据集中,FOXD1表达存在显著差异。此外,U251和U87胶质瘤细胞中FOXD1表达降低导致细胞生长延迟和集落形成受到破坏。FOXD1沉默还促进了含有核碎片的凋亡小体的产生。FOXD1表达受抑制的细胞显著降低了胶质瘤细胞的迁移能力。我们的结果表明,FOXD1可能是胶质母细胞瘤细胞行为的一种新型调节因子,有望为基因靶向胶质瘤治疗提供新的靶点。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验