Interruption of β-catenin suppresses the EGFR pathway by blocking multiple oncogenic targets in human glioma cells

Xiao, Yue; Lan, Fengming; Yang, Weidong; Yang, Yang; Han, Lei; Zhang, Anling; Liu, Ji‐Long; Zeng, Hao; Jiang, Tao; Pu, Peiyu; Kang, Chunsheng

doi:10.1016/j.brainres.2010.10.032

Cited by 91 publications

(65 citation statements)

References 34 publications

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“…Wnt/β-catenin/TCF signaling and β-catenin/TCF/LEF complex are important contributors to the development of multiple cancers including glioma [28,13,12]. The findings presented here revealed for the first time that GRβ serves as a co-activator for Wnt signaling potentiating glioma progression by interacting to TCF-4.…”

Section: Discussionmentioning

confidence: 60%

Glucocorticoid Receptor β Acts as a Co-activator of T-Cell Factor 4 and Enhances Glioma Cell Proliferation

Wang

Shi

et al. 2014

Mol Neurobiol

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We previously reported that glucocorticoid receptor β (GRβ) regulates injury-mediated astrocyte activation and contributes to glioma pathogenesis via modulation of β-catenin/ T-cell factor/Lymphoid enhancer factor (TCF/LEF) transcriptional activity. The aim of this study was to characterize the mechanism behind cross-talk between GRβ and β-catenin/TCF in the progression of glioma. Here, we reported that GRβ knock-down reduced U118 and Shg44 glioma cell proliferation in vitro and in vivo. Mechanistically, we found that GRβ knock-down decreased TCF/LEF transcriptional activity without affecting β-catenin/TCF complex. Both GRα and GRβ directly interact with TCF-4, while only GRβ is required for sustaining TCF/LEF activity under hormone-free condition. GRβ bound to the N-terminus domain of TCF-4 its influence on Wnt signaling required both ligand binding and DNA-binding domains (LBD and DBD, respectively). GRβ and TCF-4 interaction is enough to maintain the TCF/LEF activity at a high level in the absence of β-catenin stabilization.Taken together, these results suggest a novel cross-talk between GRβ and TCF-4 which regulates Wnt signaling and the proliferation in gliomas.

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Section: Discussionmentioning

confidence: 60%

Glucocorticoid Receptor β Acts as a Co-activator of T-Cell Factor 4 and Enhances Glioma Cell Proliferation

Wang

Shi

et al. 2014

Mol Neurobiol

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“…14 Conversely, inhibition of β-catenin suppressed cellular invasion in U87MG and LN229 GBM cells. 95 In addition, WNT5A was shown to induce migration in GBM cells by activating a β-catenin-independent pathway. WNT5A knockdown in glioma cells significantly inhibited the migratory capacity of these cells without affecting proliferation kinetics.…”

Section: Wnt Signaling In Gbm Stem Cells (Gscs)mentioning

confidence: 99%

“…115,116 Bioinformatic analysis with Search Tool for Retrieval of Interacting Genes/Proteins (STRING) indicated that β-catenin is associated with several genes, including Akt1, CCND1, JUN, tumor suppressors in the p53, and VEGFA. 95 Moreover, multiple signaling pathways, including the mitogen-activated protein kinase, insulin, focal adhesion and adherens junction and ErbB pathways, were proposed as β-catenin-related pathways. Based on these analyses, several studies attempted to find a relationship between the EGFR and WNT pathways.…”

Section: Cross-talk Between Wnt and Other Signaling Pathways In Gbmmentioning

confidence: 99%

WNT signaling in glioblastoma and therapeutic opportunities

Lee

Ahn

et al. 2016

Laboratory Investigation

212

182

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WNTs and their downstream effectors regulate proliferation, death, and migration and cell fate decision. Deregulation of WNT signaling is associated with various cancers including GBM, which is the most malignant primary brain cancer. In this review, we will summarize the experimental evidence supporting oncogenic roles of WNT signaling in GBM and discuss current progress in the targeting of WNT signaling as an anti-cancer approach. In particular, we will focus on (1) genetic and epigenetic alterations that lead to aberrant WNT pathway activation in GBM, (2) WNT-mediated control of GBM stem cell maintenance and invasion, and (3) cross-talk between WNT and other signaling pathways in GBM. We will then review the discovery of agents that can inhibit WNT signaling in preclinical models and the current status of human clinical trials.

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“…More and more studies have reported that β-catenin/Tcf-4 pathway played an important role in the pathogenesis of glioma (15,16). Herein, we wanted to detect the transcription activities of β-catenin/Tcf-4 in glioma after treatment by miR-27b inhibitor.…”

Section: Mir-27 Low-expression Reduces Transcription Activities Of β-mentioning

confidence: 99%

Expression and function of miR-27b in human glioma

Chen

Li²,

Han³

et al. 2011

Oncol Rep

Self Cite

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Abstract. Our previous miRNAs profiling study showed that miR-27b was up-regulated in glioma cells compared with H4 low grade astrocytoma cells. However, the main function of miR-27b in glioma in not known yet. The aim of this study was to investigate the expression and function of miR-27b in the pathogenesis of glioma. Real-time PCR showed that miR-27b was up-regulated in glioma samples and glioma cells. Downregulation of miR-27b triggered growth inhibition, induced apoptosis and inhibited invasion in glioma cells. Furthermore, TOPflash luciferase activity was decreased significantly, while FOPflash luciferase did not change significantly. In addition, Western blot assay showed that STAT3, c-myc and cyclin D1 were knocked down after treatment with miR-27b inhibitor. These findings suggest that aberrantly up-regulated miR-27b may be one of the critical factors that contribute to malignancy in human gliomas.

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Interruption of β-catenin suppresses the EGFR pathway by blocking multiple oncogenic targets in human glioma cells

Cited by 91 publications

References 34 publications

Glucocorticoid Receptor β Acts as a Co-activator of T-Cell Factor 4 and Enhances Glioma Cell Proliferation

Glucocorticoid Receptor β Acts as a Co-activator of T-Cell Factor 4 and Enhances Glioma Cell Proliferation

WNT signaling in glioblastoma and therapeutic opportunities

Expression and function of miR-27b in human glioma

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