FoxG1 facilitates proliferation and inhibits differentiation by downregulating FoxO/Smad signaling in glioblastoma

Wang, Lei; Wang, Jingchao; Jin, Tong‐Shou; Zhou, Yi; Chen, Qianxue

doi:10.1016/j.bbrc.2018.08.118

Cited by 26 publications

(22 citation statements)

References 47 publications

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“…The knockdown of FOXG1, in turn, had the opposite effect. These results suggest that the shortening of the G2/M arrest via repression of CDKN1A and cyclin B1 primarily accounts for the accelerated cell cycle and proliferation in the presence of FOXG1 (Figure 1; Wang et al, 2018).…”

Section: Regulation Of Core Cell Cycle and Methyltransferase Gene Expmentioning

confidence: 86%

“…Studies into the means by which FOXG1 regulates the cell cycle used key markers CDKN1A and CCNB1/cyclin B1 and demonstrated that overexpression of FOXG1 repressed both CDKN1A and cyclin B1 expression and decreased the proportion of cells in G2 phase (Figure 1; Wang et al, 2018). The knockdown of FOXG1, in turn, had the opposite effect.…”

Section: Regulation Of Core Cell Cycle and Methyltransferase Gene Expmentioning

confidence: 99%

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Transcription and Beyond: Delineating FOXG1 Function in Cortical Development and Disorders

Hou

hAilín

Vogel

et al. 2020

Front. Cell. Neurosci.

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Forkhead Box G1 (FOXG1) is a member of the Forkhead family of genes with non-redundant roles in brain development, where alteration of this gene's expression significantly affects the formation and function of the mammalian cerebral cortex. FOXG1 haploinsufficiency in humans is associated with prominent differences in brain size and impaired intellectual development noticeable in early childhood, while homozygous mutations are typically fatal. As such, FOXG1 has been implicated in a wide spectrum of congenital brain disorders, including the congenital variant of Rett syndrome, infantile spasms, microcephaly, autism spectrum disorder (ASD) and schizophrenia. Recent technological advances have yielded greater insight into phenotypic variations observed in FOXG1 syndrome, molecular mechanisms underlying pathogenesis of the disease, and multifaceted roles of FOXG1 expression. In this review, we explore the emerging mechanisms of FOXG1 in a range of transcriptional to posttranscriptional events in order to evolve our current view of how a single transcription factor governs the assembly of an elaborate cortical circuit responsible for higher cognitive functions and neurological disorders.

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Section: Regulation Of Core Cell Cycle and Methyltransferase Gene Expmentioning

confidence: 86%

Section: Regulation Of Core Cell Cycle and Methyltransferase Gene Expmentioning

confidence: 99%

Transcription and Beyond: Delineating FOXG1 Function in Cortical Development and Disorders

Hou

hAilín

Vogel

et al. 2020

Front. Cell. Neurosci.

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“…Among these genes, several had been previously studied in various tumors. Some studies have suggested that FoxG1 functions as an oncogene by promoting proliferation, as well as inhibiting differential responses in glioblastoma, by downregulating FoxO/Smad signaling (31). Moreover, low FoxG1 and high Olig-2 labeling indices define a prognostically favorable subset in IDH-mutant gliomas (32).…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Profiling Stratifies IDH-Wildtype Glioblastoma With Distinct Prognoses

Liu

et al. 2019

Front. Oncol.

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Objectives: In the present study, we aimed to determine the candidate genes that may function as biomarkers to further distinguish patients with isocitrate dehydrogenase (IDH)-wildtype glioblastoma (GBM), which are heterogeneous with respect to clinical outcomes. Materials and Methods: We selected 41 candidate genes associated with overall survival (OS) using univariate Cox regression from IDH-wildtype GBM patients based on RNA sequencing (RNAseq) expression data from the Chinese Glioma Genome Atlas (CGGA, n = 105) and The Cancer Genome Atlas (TCGA, n = 139) cohorts. Next, a sevengene-based risk signature was formulated according to Least Absolute Shrinkage and Selection Operator (LASSO) regression algorithm in the CGGA RNAseq database as a training set, while another 525 IDH-wildtype GBM patient TCGA datasets, consisting of RNA sequencing and microarray data, were used for validation. Patient survival in the low-and high-risk groups was calculated using Kaplan-Meier survival curve analysis and the log-rank test. Uni-and multivariate Cox regression analysis was used to assess the prognosis value. Gene oncology (GO) and gene set enrichment analysis (GSEA) were performed for the functional analysis of the seven-gene-based risk signature. Results: We developed a seven-gene-based signature, which allocated each patient to a risk group (low or high). Patients in the high-risk group had dramatically shorter overall survival than their low-risk counterparts in three independent cohorts. Univariate and multivariate analysis showed that the seven-gene signature remained an independent prognostic factor. Moreover, the seven-gene risk signature exhibited a striking prognostic validity, with AUC of 78.4 and 73.9%, which was higher than for traditional "age" (53.7%, 62.4%) and "GBM sub-type" (57.7%, 52.9%) in the CGGA-and TCGA-RNAseq databases, respectively. Subsequent bioinformatics analysis predicted that the sevengene signature was involved in the inflammatory response, immune response, cell adhesion, and apoptotic process. Conclusions: Our findings indicate that the seven-gene signature could be a potential prognostic biomarker. This study refined the current classification system of IDH-wildtype GBM and may provide a novel perspective for the research and individual therapy of IDH-wildtype GBM.

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“…26 FOXG1 expression was also found to have a positive correlation with the disease progression of glioblastoma multiforme, which is one of the most common malignancies of the brain. 27 Previous research demonstrated that the decreased expression of FOXG1 inhibited the tumor growth in a xenograft mouse model of medulloblastoma. 17 The downregulation of FOXG1 has been proven to prevent the occurrence of carcinogenicity of brain tumor-initiating cells.…”

Section: Discussionmentioning

confidence: 99%

microRNA -378a-3p Restrains the Proliferation of Retinoblastoma Cells but Promotes Apoptosis of Retinoblastoma Cells via Inhibition of FOXG1

Zhang

2020

Invest. Ophthalmol. Vis. Sci.

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FoxG1 facilitates proliferation and inhibits differentiation by downregulating FoxO/Smad signaling in glioblastoma

Abstract: Our findings suggest that FoxG1 functions as an onco-factor by promoting proliferation, as well as inhibiting differential responses in glioblastoma by downregulating FoxO/Smad signaling.

Cited by 26 publications

References 47 publications

Transcription and Beyond: Delineating FOXG1 Function in Cortical Development and Disorders

Transcription and Beyond: Delineating FOXG1 Function in Cortical Development and Disorders

Gene Expression Profiling Stratifies IDH-Wildtype Glioblastoma With Distinct Prognoses

microRNA -378a-3p Restrains the Proliferation of Retinoblastoma Cells but Promotes Apoptosis of Retinoblastoma Cells via Inhibition of FOXG1

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