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

被引:37
作者
Gao, Yuan-Feng [1 ,2 ,3 ]
Zhu, Tao [1 ,2 ,3 ]
Mao, Xiao-Yuan [1 ,2 ,3 ]
Mao, Chen-Xue [1 ,2 ,3 ]
Li, Ling [1 ,2 ,3 ]
Yin, Ji-Ye [1 ,2 ,3 ]
Zhou, Hong-Hao [1 ,2 ,3 ]
Liu, Zhao-Qian [1 ,2 ,3 ]
机构
[1] Cent S Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China
[2] Cent S Univ, Inst Clin Pharmacol, Changsha 410078, Hunan, Peoples R China
[3] Cent S Univ, Hunan Key Lab Pharmacogenet, Changsha 410078, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
glioma; FOXD1; proliferation; migration; prognostic value; TRANSCRIPTION FACTOR; GENE FAMILY; CANCER; FOXD1; PROTEINS; CLONING; KIDNEY; HEAD; BF-2;
D O I
10.3892/or.2017.5344
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:1196 / 1202
页数:7
相关论文
共 31 条
[1]   Foxm1 transcription factor is required for lung fibrosis and epithelial-to-mesenchymal transition [J].
Balli, David ;
Ustiyan, Vladimir ;
Zhang, Yufang ;
Wang, I-Ching ;
Masino, Alex J. ;
Ren, Xiaomeng ;
Whitsett, Jeffrey A. ;
Kalinichenko, Vladimir V. ;
Kalin, Tanya V. .
EMBO JOURNAL, 2013, 32 (02) :231-244
[2]   FOXD1 promotes nephron progenitor differentiation by repressing decorin in the embryonic kidney [J].
Fetting, Jennifer L. ;
Guay, Justin A. ;
Karolak, Michele J. ;
Iozzo, Renato V. ;
Adams, Derek C. ;
Maridas, David E. ;
Brown, Aaron C. ;
Oxburgh, Leif .
DEVELOPMENT, 2014, 141 (01) :17-27
[3]   The Forkhead Transcription Factor, Foxd1, Is Necessary for Pituitary Luteinizing Hormone Expression in Mice [J].
Gumbel, Jason H. ;
Patterson, Elizabeth M. ;
Owusu, Sarah A. ;
Kabat, Brock E. ;
Jung, Deborah O. ;
Simmons, Jasmine ;
Hopkins, Torin ;
Ellsworth, Buffy S. .
PLOS ONE, 2012, 7 (12)
[4]   Emerging role of combination of all-trans retinoic acid and interferon-gamma as chemoimmunotherapy in the management of human glioblastoma [J].
Haque, Azizul ;
Banik, Naren L. ;
Ray, Swapan K. .
NEUROCHEMICAL RESEARCH, 2007, 32 (12) :2203-2209
[5]   EXPRESSION OF WINGED HELIX GENES, BF-1 AND BF-2, DEFINE ADJACENT DOMAINS WITHIN THE DEVELOPING FOREBRAIN AND RETINA [J].
HATINI, V ;
TAO, WF ;
LAI, E .
JOURNAL OF NEUROBIOLOGY, 1994, 25 (10) :1293-1309
[6]   Essential role of stromal mesenchyme in kidney morphogenesis revealed by targeted disruption of Winged Helix transcription factor BF-2 [J].
Hatini, V ;
Huh, SO ;
Herzlinger, D ;
Soares, VC ;
Lai, E .
GENES & DEVELOPMENT, 1996, 10 (12) :1467-1478
[7]   Foxd1 is required for proper formation of the optic chiasm [J].
Herrera, E ;
Marcus, R ;
Li, S ;
Williams, SE ;
Erskine, L ;
Lai, E ;
Mason, C .
DEVELOPMENT, 2004, 131 (22) :5727-5739
[8]   AF6q21, a novel partner of the MLL gene in t(6;11)(q21;q23), defines a forkhead transcriptional factor subfamily [J].
Hillion, J ;
LeConiat, M ;
Jonveaux, P ;
Berger, R ;
Bernard, OA .
BLOOD, 1997, 90 (09) :3714-3719
[9]   Fate Tracing Reveals the Pericyte and Not Epithelial Origin of Myofibroblasts in Kidney Fibrosis [J].
Humphreys, Benjamin D. ;
Lin, Shuei-Liong ;
Kobayashi, Akio ;
Hudson, Thomas E. ;
Nowlin, Brian T. ;
Bonventre, Joseph V. ;
Valerius, M. Todd ;
McMahon, Andrew P. ;
Duffield, Jeremy S. .
AMERICAN JOURNAL OF PATHOLOGY, 2010, 176 (01) :85-97
[10]  
Kaestner KH, 2000, GENE DEV, V14, P142