ArticleOncology reviews2020
Elucidating the pathogenic and biomarker potentials of FOXG1 in glioblastoma.
Article in Oncology reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- FOXG1 interaction with SATB2 promotes autophagy to alleviate neuroinflammation and mechanical abnormal pain in rats with lumbar disc herniation.Annals of medicine · 2024Article
- FoxG1 as a Potential Therapeutic Target for Alzheimer's Disease: Modulating NLRP3 Inflammasome via AMPK/mTOR Autophagy Pathway.Cellular and molecular neurobiology · 2024Article
- Article
- The Role of FoxG1 in the Inner Ear.Frontiers in cell and developmental biology · 2020Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GB) is an extremely pugnacious brain cancer originating from neural stem (NS) cell-like cells. Forkhead box G1 (FOXG1; previously recognized as BF-1, qin, Chicken Brain Factor 1, or XBF-1 and renamed FOXG1 for mouse and human, and FoxG1 for other chordates) is an evolutionary preserved transcription factor driven from the forkhead box group of proteins FOXG1 modulates the speed of neurogenesis by maintaining progenitor cells in a proliferative mode as well as obstructing their differentiation into neurons during the initial periods of cortical formation. FOXG1 has been implicated in the formation of central nervous system (CNS) tumors and precisely GBs. Pathophysiologically, joint actions of FOXG1 and phosphatidylinositol- 3-kinases (PI3K) intermediate in intrinsic resistance of human GB cells to transforming growth factor-beta (TGF-β) stimulation of cyclin-dependent kinase inhibitor 1(p21Cip1) as well as growth inhibition. FOXG1 and NOTCH signaling pathways may functionally interrelate at different stages to facilitate gliomagenesis. Furthermore, FoxG1 actively contributed to the formation of transcription suppression complexes with corepressors of the Groucho/transducin-like Enhancer of split (Gro/TLEs). Also, FOXG1 was stimulated by Gro/TLE1 and abridged by Grg6. FOXG1 silencing in brain tumor-initiating cells (BTICs) also resulted in diminished secretion of markers characteristic undifferentiated natural neural stem/progenitor cells (NSPC) states, such as Oligodendrocyte transcription factor (OLIG2), (sex determining region Y)-box 2. (SOX2) and B lymphoma Mo-MLV insertion region 1 homolog (BMI1). This review therefore focuses on the pathogenic and biomarker potentials of FOXG1 in GB.
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Registered trials
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