Compounds > 4-(5-benzo(1-3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide

4-(5-benzo(1-3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide and Glioblastoma

4-(5-benzo(1-3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide has been researched along with Glioblastoma* in 1 studies

Other Studies

1 other study(ies) available for 4-(5-benzo(1-3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide and Glioblastoma

Article	Year
Autocrine TGF-beta signaling maintains tumorigenicity of glioma-initiating cells through Sry-related HMG-box factors. Cell stem cell, 2009, Nov-06, Volume: 5, Issue:5 Despite aggressive surgery, radiotherapy, and chemotherapy, treatment of malignant glioma remains formidable. Although the concept of cancer stem cells reveals a new framework of cancer therapeutic strategies against malignant glioma, it remains unclear how glioma stem cells could be eradicated. Here, we demonstrate that autocrine TGF-beta signaling plays an essential role in retention of stemness of glioma-initiating cells (GICs) and describe the underlying mechanism for it. TGF-beta induced [corrected] expression of Sox2, a stemness gene, and this induction was mediated by Sox4, a direct TGF-beta target gene. Inhibitors of TGF-beta signaling drastically deprived tumorigenicity of GICs by promoting their differentiation, and these effects were attenuated in GICs transduced with Sox2 or Sox4. Furthermore, GICs pretreated with TGF-beta signaling inhibitor exhibited less lethal potency in intracranial transplantation assay. These results identify an essential pathway for GICs, the TGF-beta-Sox4-Sox2 pathway, whose disruption would be a therapeutic strategy against gliomas. Topics: Aged; Animals; Benzamides; Brain Neoplasms; Cell Differentiation; Cells, Cultured; Dioxoles; Female; Glioblastoma; Humans; Male; Mice; Mice, Nude; Middle Aged; Neoplasm Transplantation; Neoplastic Stem Cells; Receptors, Transforming Growth Factor beta; Signal Transduction; SOX Transcription Factors; SOXB1 Transcription Factors; SOXC Transcription Factors; Transforming Growth Factor beta	2009

Article

Year

Autocrine TGF-beta signaling maintains tumorigenicity of glioma-initiating cells through Sry-related HMG-box factors.

Cell stem cell, 2009, Nov-06, Volume: 5, Issue:5

Despite aggressive surgery, radiotherapy, and chemotherapy, treatment of malignant glioma remains formidable. Although the concept of cancer stem cells reveals a new framework of cancer therapeutic strategies against malignant glioma, it remains unclear how glioma stem cells could be eradicated. Here, we demonstrate that autocrine TGF-beta signaling plays an essential role in retention of stemness of glioma-initiating cells (GICs) and describe the underlying mechanism for it. TGF-beta induced [corrected] expression of Sox2, a stemness gene, and this induction was mediated by Sox4, a direct TGF-beta target gene. Inhibitors of TGF-beta signaling drastically deprived tumorigenicity of GICs by promoting their differentiation, and these effects were attenuated in GICs transduced with Sox2 or Sox4. Furthermore, GICs pretreated with TGF-beta signaling inhibitor exhibited less lethal potency in intracranial transplantation assay. These results identify an essential pathway for GICs, the TGF-beta-Sox4-Sox2 pathway, whose disruption would be a therapeutic strategy against gliomas.

Topics: Aged; Animals; Benzamides; Brain Neoplasms; Cell Differentiation; Cells, Cultured; Dioxoles; Female; Glioblastoma; Humans; Male; Mice; Mice, Nude; Middle Aged; Neoplasm Transplantation; Neoplastic Stem Cells; Receptors, Transforming Growth Factor beta; Signal Transduction; SOX Transcription Factors; SOXB1 Transcription Factors; SOXC Transcription Factors; Transforming Growth Factor beta

2009