Silencing of Forkhead box D1 inhibits proliferation and migration in glioma cells
Silencing of Forkhead box D1 inhibits proliferation and migration in glioma cells
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DOI：
10.3892/or.2017.5344
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发表时间：
2017-02-01
期刊：
影响因子：
4.2
通讯作者：
Liu, Zhao-Qian
中科院分区：
文献类型：
--
作者：
Gao, Yuan-Feng;Zhu, Tao;Liu, Zhao-Qian
尽管叉头盒转录因子在各种癌症的发生和进展中发挥着广泛作用，但人们对其在神经胶质瘤中的作用知之甚少。我们检查了 Forkhead box D1 (FOXD1) 在神经胶质瘤细胞行为中的表达和功能，发现 FOXD1 上调并与神经胶质瘤分级直接相关。数据分析还揭示了基因表达谱（GSE4290 和 GSE7696）和 TCGA 数据集的 FOXD1 表达存在显着差异。此外，U251和U87神经胶质瘤细胞中FOXD1表达的降低导致细胞生长延迟和集落形成破坏。 FOXD1沉默还促进含有核碎片的凋亡小体的产生。 FOXD1 表达受到抑制的细胞显着减少了神经胶质瘤细胞的迁移。我们的结果表明，FOXD1 可能作为胶质母细胞瘤细胞行为的新型调节剂，为基因靶向胶质瘤治疗提供新的靶点。
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.