β-Catenin overexpression in malignant glioma and its role in proliferation and apoptosis in glioblastma cells

Liu, Xiangrong; Wang, Lei; Zhao, Shichao; Ji, Xunming; Luo, Yumin; Li, Feng

doi:10.1007/s12032-010-9476-5

Cited by 92 publications

(86 citation statements)

References 22 publications

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“…Furthermore, the proliferation of glioma cells may be inhibited by targeting specific molecules using Wnt2 and β-catenin small interfering RNAs (18,47,48). β-catenin expression demonstrates an association with the poor prognosis of patients with GBM, including shorter survival times (19,49). The aforementioned previous studies are in line with the data presented in the R2 Platform, in which patients with a high expression of Wnt5a, Wnt2b, FZD2, FZD6 and FZD7 exhibited a worse overall survival time.…”

Section: Discussionsupporting

confidence: 82%

“…Although the expression of Wnt/β-catenin signaling pathway members in glioma has been demonstrated previously (15,(18)(19)(20), there is a lack of studies that have systematically investigated the expression of Wnt signaling. In order to comprehensively characterize the expression of Wnt signaling in glioma tissues, the R2: Genomics Analysis and Visualization Platform database was interrogated, which revealed that, in patients with glioma, the median mRNA expression levels of Wnt2b, Wnt5a, FZD1-7 were increased compared with other Wnt pathway members (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Regarding β-catenin, Liu et al (19) and Shi et al (20) demonstrated that mRNA and protein levels increased with an increase in astrocytic glioma pathological grade. In contrast, Pu et al (18) reported that the mRNA expression of β-catenin in gliomas analyzed using RT-qPCR did not exhibit any change, which is consistent with the results of the present study.…”

Section: Discussionmentioning

confidence: 99%

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Expression profile and clinical significance of Wnt signaling in human gliomas

Zhang

Geng

et al. 2017

Oncol Lett

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Abstract. Wnt signaling has been identified as a critical regulator of human tumor development in vitro. However, there remains a lack of studies systematically examining the expression pattern and clinical relevance of the core molecules of Wnt signaling in glioma tissues. In the present study, it was identified that the mRNA expression levels of Wnt3a and 5a, and their receptors frizzled 2, 6 and 7 increased, whereas Wnt7b was markedly decreased in glioma relative to non-tumor tissue. The mRNA levels of β-catenin, adenomatous polyposis coli gene product, glycogen synthase kinase 3β (GSK3β) and AXIN1 and its target genes cyclin D1 and AXIN2 did not differ. Similarly, the protein levels of Wnt2b, 3a and 5a were increased in gliomas, while β-catenin, GSK3β and cyclin D1 were not. Furthermore, based on data from the R2: Genomics Analysis and Visualization Platform, the expression of Wnt2b and 5a, and frizzled 2, 6 and 7 were highly associated with the prognosis of patients with glioma. Taken together, the results of the present study demonstrate that β-catenin is not upregulated in gliomas and that the Wnt signaling pathway may promote glioma development via noncanonical or alternative pathways.

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Section: Discussionsupporting

confidence: 82%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Expression profile and clinical significance of Wnt signaling in human gliomas

Zhang

Geng

et al. 2017

Oncol Lett

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“…The lysis buffer was used as previously described. 13 The tissues and cells were homogenized and centrifuged at 12 000 rpm for 30 minutes at 4°C, and then the supernatant was collected. Protein concentration was determined by a bicinchoninic acid protein assay kit (Pierce, Rockford, IL) using BSA as the standard.…”

Section: Western Blot Analysismentioning

confidence: 99%

MicroRNA-124–Mediated Regulation of Inhibitory Member of Apoptosis-Stimulating Protein of p53 Family in Experimental Stroke

Liu

Zhao

et al. 2013

Stroke

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Background and Purpose-p53-mediated neuronal death is a central pathway of stroke pathophysiology, but its mechanistic details remain unclear. Here, we identified a novel microRNA mechanism that downregulation of inhibitory member of the apoptosis-stimulating proteins of p53 family (iASPP) by the brain-specific microRNA-124 (miR-124) promotes neuronal death after cerebral ischemia. Methods-In a mouse model of focal permanent cerebral ischemia, the expression of iASPP and miR-124 was quantified by reverse transcription quantitative real-time polymerase chain reaction, immunofluorescence staining, and Western blot. Luciferase reporter assay was used to validate whether miR-124 can directly bind to the 3′-untranslated region of iASPP mRNA. To evaluate the role of miR-124, miR-124 mimic and its inhibitor were transfected into Neuro-2a cells and C57 mice. Results-There was no change in the iASPP mRNA level in cerebral ischemia. However, iASPP protein was remarkably decreased, with a concurrent elevation in miR-124 level. Furthermore, miR-124 can bind to the 3′-untranslated region of iASPP in 293T cells and downregulate its protein levels in Neuro-2a cells. In vivo, infusion of miR-124 decreased brain levels of iASPP, whereas inhibition of miR-124 enhanced iASPP levels and significantly reduced infarction in mouse focal cerebral ischemia. Conclusions-These data demonstrate that p53-mediated neuronal cell death after stroke can be nontranscriptionally regulated by a novel mechanism involving suppression of endogenous cell death inhibitors by miR-124. Further dissection of microRNA regulatory mechanisms may lead to new therapeutic opportunities for preventing neuronal death after stroke.

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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

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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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β-Catenin overexpression in malignant glioma and its role in proliferation and apoptosis in glioblastma cells

Cited by 92 publications

References 22 publications

Expression profile and clinical significance of Wnt signaling in human gliomas

Expression profile and clinical significance of Wnt signaling in human gliomas

MicroRNA-124–Mediated Regulation of Inhibitory Member of Apoptosis-Stimulating Protein of p53 Family in Experimental Stroke

Expression and function of miR-27b in human glioma

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