Driver or passenger effects of augmented <i>c-Myc</i> and <i>Cdc20</i> in gliomagenesis

Ji, Ping; Zhou, Xinhui; Li, Qun; Fuller, Gregory N.; Phillips, Lynette M.; Zhang, Wei

doi:10.18632/oncotarget.8080

Cited by 5 publications

(4 citation statements)

References 37 publications

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“…It was reported that CDC20 was a critical regulator of tumor-initiating cell proliferation and survival of glioblastoma cells (35). Combining the findings of other studies, CDC20 was found to play a role in cell cycle progression, apoptosis and brain development, and these findings indicated that it may be a potential novel target for therapeutic intervention in brain tumors, particularly MB (36,37). In addition, the RNA levels of CDC20 and MAD2L1 were associated with glioma grade, which suggested a clinical benefit as a biomarker (38).…”

Section: Discussionsupporting

confidence: 60%

Examining the biomarkers and molecular mechanisms of medulloblastoma based on bioinformatics analysis

et al. 2019

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Medulloblastoma (MB) is the most common malignant brain tumor in children. The aim of the present study was to predict biomarkers and reveal their potential molecular mechanisms in MB. The gene expression profiles of GSE35493, GSE50161, GSE74195 and GSE86574 were downloaded from the Gene Expression Omnibus (GEO) database. Using the Limma package in R, a total of 1,006 overlapped differentially expressed genes (DEGs) with the cut-off criteria of P<0.05 and |log 2 fold-change (FC)|>1 were identified between MB and normal samples, including 540 upregulated and 466 downregulated genes. Furthermore, the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were also performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID) online tool to analyze functional and pathway enrichment. The Search Tool for Retrieval of Interacting Genes database was subsequently used to construct a protein-protein interaction (PPI) network and the network was visualized in Cytoscape. The top 11 hub genes, including CDK1, CCNB1, CCNB2, PLK1, CDC20, MAD2L1, AURKB, CENPE, TOP2A, KIF2C and PCNA, were identified from the PPI network. The survival curves for hub genes in the dataset GSE85217 predicted the association between the genes and survival of patients with MB. The top 3 modules were identified by the Molecular Complex Detection plugin. The results indicated that the pathways of DEGs in module 1 were primarily enriched in cell cycle, progesterone-mediated oocyte maturation and oocyte meiosis; and the most significant functional pathways in modules 2 and 3 were primarily enriched in mismatch repair and ubiquitin-mediated proteolysis, respectively. These results may help elucidate the pathogenesis and design novel treatments for MB.

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Section: Discussionsupporting

confidence: 60%

Examining the biomarkers and molecular mechanisms of medulloblastoma based on bioinformatics analysis

et al. 2019

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“…Moreover, using an orthotopic xenograft model overexpression of Cdc20 enhanced the GSCs to generate brain tumors, whereas depletion of Cdc20 retarded the GSCs to develop brain tumors [ 39 ]. Strikingly, it has been reported that Cdc20 induced the proliferation of primary glial progenitor cells [ 40 ]. Some studies showed that rottlerin inhibited cancer cell growth and induced apoptosis in a variety of human cancers [ 13 , 14 , 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

Rottlerin inhibits cell growth and invasion via down-regulation of Cdc20 in glioma cells

et al. 2016

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Rottlerin, isolated from a medicinal plant Mallotus phillippinensis, has been demonstrated to inhibit cellular growth and induce cytoxicity in glioblastoma cell lines through inhibition of calmodulin-dependent protein kinase III. Emerging evidence suggests that rottlerin exerts its antitumor activity as a protein kinase C inhibitor. Although further studies revealed that rottlerin regulated multiple signaling pathways to suppress tumor cell growth, the exact molecular insight on rottlerin-mediated tumor inhibition is not fully elucidated. In the current study, we determine the function of rottlerin on glioma cell growth, apoptosis, cell cycle, migration and invasion. We found that rottlerin inhibited cell growth, migration, invasion, but induced apoptosis and cell cycle arrest. Mechanistically, the expression of Cdc20 oncoprotein was measured by the RT-PCR and Western blot analysis in glioma cells treated with rottlerin. We observed that rottlerin significantly inhibited the expression of Cdc20 in glioma cells, implying that Cdc20 could be a novel target of rottlerin. In line with this, over-expression of Cdc20 decreased rottlerin-induced cell growth inhibition and apoptosis, whereas down-regulation of Cdc20 by its shRNA promotes rottlerin-induced anti-tumor activity. Our findings indicted that rottlerin could exert its tumor suppressive function by inhibiting Cdc20 pathway which is constitutively active in glioma cells. Therefore, down-regulation of Cdc20 by rottlerin could be a promising therapeutic strategy for the treatment of glioma.

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“…Due to its role as methyltransferase, EZH2 acts as a major suppressor of tumor suppressor expression such as p19, p57, and E‐cadherin . Protein kinase B (AKT) is an oncogenic kinase that interferes with cellular transformation, angiogenesis, invasion, and migration in tumor cells . Overexpression of AKT significantly increases at the level of EZH2 S21 phosphorylation .…”

Section: Effects Of Melatonin On Signaling Pathwaysmentioning

confidence: 99%

“…One major challenge in the development of new therapies is the heterogeneity of tumor at the cellular and molecular levels . Multiple studies indicated excessive expression of a large number of possible oncogenes in GBM . The main goal of cancer treatment is to find new biomarkers that can suppress cancer cells without damaging normal cells .…”

Section: Introductionmentioning

confidence: 99%

The effects of melatonin on signaling pathways and molecules involved in glioma

Neamati

Asemi

2019

Fundamemntal Clinical Pharma

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Glioblastoma is one of the most common brain tumors with high invasion and malignancy. Despite extensive research in this area and the use of new and advanced therapies, the survival rate in this disease is very low. In addition, resistance to treatment has also been observed in this disease. One of the reasons for rapid progression and failure in treatment for this disease is the presence of a class of cells with high proliferation and high differentiation, a class called glioblastoma stem‐like cells shown as being the source of glioblastoma tumors. It has been reported that several oncogenes are expressed in this disease. One important issue in recognizing the pathogenesis of this disease, and which could improve the treatment process, is the identification of involved oncogenes as well as molecules that affect the reduction of the expression of these oncogenes. Melatonin regulates the biological rhythm and inhibits the proliferation of malignant glioma cells due to antioxidant and anti‐apoptotic effects. Melatonin has been considered in biological processes and in signaling pathways involved in the development of glioma. The aim of this review is to investigate the effects of melatonin on signaling pathways and molecules involved in the progression of glioma.

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Driver or passenger effects of augmented c-Myc and Cdc20 in gliomagenesis

Cited by 5 publications

References 37 publications

Examining the biomarkers and molecular mechanisms of medulloblastoma based on bioinformatics analysis

Examining the biomarkers and molecular mechanisms of medulloblastoma based on bioinformatics analysis

Rottlerin inhibits cell growth and invasion via down-regulation of Cdc20 in glioma cells

The effects of melatonin on signaling pathways and molecules involved in glioma

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