Myc inhibition is effective against glioma and reveals a role for Myc in proficient mitosis

Annibali, Daniela; Whitfield, Jonathan R.; Favuzzi, Emilia; Jauset, Toni; Serrano, Erika; Cuartas, Isabel; Redondo-Campos, Sara; Folch, Gerard; Gonzàlez-Juncà, Alba; Sodir, Nicole M.; Massó-Vallés, Daniel; Beaulieu, Marie-Ève; Swigart, Lamorna Brown; Gee, Margaret M. Mc; Somma, Maria Patrizia; Nasi, Sergio; Seoane, Joan; Evan, Gérard I.; Soucek, Laura

doi:10.1038/ncomms5632

Cited by 161 publications

(147 citation statements)

References 31 publications

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“…USP28 overexpression could deubiquitinate FBW7 ....................................................................................................................... through deubiquitination of their substrates such as MYC, because USP28 is a member of the ubiquitin-specific protease family. 9,22 In this study, USP28 overexpression significantly increased MYC expression, whereas USP28 knockdown produced an opposite effect in glioma cells. The inhibition of MYC by siRNA reversed the induction of USP28 on glioma cell proliferation.…”

Section: Discussionmentioning

confidence: 89%

Ubiquitin-specific protease 28 is overexpressed in human glioblastomas and contributes to glioma tumorigenicity by regulating MYC expression

Wang

Song

Xue

et al. 2015

Exp Biol Med (Maywood)

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The transcription factor MYC, which is dysregulated in the majority of gliomas, is difficult to target directly. Deubiquitinase ubiquitin-specific protease 28 (USP28) stabilizes oncogenic factors, including MYC. However, the contribution of USP28 in tumorigenesis, particularly in glioma, is unknown. Here, we determined the expression of USP28 and assessed its clinical significance in human glioma. We found that USP28 is overexpressed in human glioma but not in normal brain tissue. The level of USP28 protein expression in human glioma tissues was directly correlated with glioma grade. Meanwhile, the level of USP28 protein expression in human glioblastoma tissues was inversely correlated with patient survival. Enforced USP28 expression promotes SW1783 glioma cell proliferation. Moreover, gliomas that arose from USP28-transfected SW1783 cells displayed tumorigenicity in nude mouse model systems. Inhibition of USP28 expression in glioblastoma U373 cells suppressed anchorage-independent growth in vitro and tumorigenicity in vivo. Furthermore, USP28 regulates the expression of MYC protein, which is essential in USP28-induced cell growth in glioma cells. These results showed that USP28 is overexpressed in human glioblastomas and it contributes to glioma tumorigenicity. Therefore, USP28 could be a new target of therapy for human malignant glioma.

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Section: Discussionmentioning

confidence: 89%

Ubiquitin-specific protease 28 is overexpressed in human glioblastomas and contributes to glioma tumorigenicity by regulating MYC expression

Wang

Song

Xue

et al. 2015

Exp Biol Med (Maywood)

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“…Mice expressing OmoMYC in a doxycycline-inducible manner display rapid regression of lung adenocarcinomas, glioblastomas and pancreatic tumors but show only mild and fully reversible effects on proliferation in normal tissues 9,17,18 . As consequence, intermittent induction of OmoMYC ("metronomic treatment") enables long-term suppression of tumor growth arguing that therapeutic strategies that mimic OmoMYC may have significant efficacy for the treatment of human tumors 19 .…”

Section: Introductionmentioning

confidence: 99%

OmoMYC blunts promoter invasion by oncogenic MYC to inhibit gene expression characteristic of MYC-dependent tumors

et al. 2016

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“…Among the factors and pathways implicated in glioma development and growth, the kinases phosphoinositide 3-kinase and mitogen-activated protein kinase are among the most studied (Daniel et al, 2014). Annibali et al, (2014) found that Myc inhibition reduces proliferation, increases apoptosis, and, remarkably, elicits the formation of multinucleated cells that then arrest or die by mitotic catastrophe, revealing a new role for Myc in the proficient division of glioma cells. Some results confirmed that PIK3CA mutations occurred in a significant number of human glioblastomas, making it a promising target for therapy, particularly for primary glioblastomas (Weber et al, 2011;Derakhshandeh-Peykar et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Analysis of the gene-protein interaction network in glioma

Zhou

Wj²,

Zhuang

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Glioma is the most aggressive type of brain tumor. Great progress has been achieved in glioma treatment, but the protein-protein interaction networks underlining glioma are poorly understood. We identified the protein-protein interaction network for glioma based on gene expression and predicted biological pathways underlying the molecular complexes in the network. Genes involved in glioma were selected from the Online Mendelian Inheritance in Man (OMIM) database. A literature search was performed using the Agilent Literature Search plugin, and Cytoscape was used to establish a protein-protein interaction network. The molecular complexes in the network were detected using the Clusterviz plugin, and pathway enrichment of molecular complexes was performed using DAVID online. There were 378 glioma genes in the OMIM database. The protein-protein interaction network in glioma contained 1814 nodes, 6471 edges, and 8 molecular complexes. There were 17 pathways (false discovery rate <1), which were related to cytokinecytokine receptor interaction, Toll-like receptor signaling pathway, chemokine signaling pathway, oocyte meiosis, progesterone-mediated oocyte maturation, transmembrane transport of small molecules, metabolism of amino acids, and notch signaling pathway, among others. Our results provide a bioinformatic 14197 Gene-protein interaction network analysis in glioma ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 14196-14206 (2015) foundation for further studies of the mechanisms of glioma.

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Myc inhibition is effective against glioma and reveals a role for Myc in proficient mitosis

Cited by 161 publications

References 31 publications

Ubiquitin-specific protease 28 is overexpressed in human glioblastomas and contributes to glioma tumorigenicity by regulating MYC expression

Ubiquitin-specific protease 28 is overexpressed in human glioblastomas and contributes to glioma tumorigenicity by regulating MYC expression

OmoMYC blunts promoter invasion by oncogenic MYC to inhibit gene expression characteristic of MYC-dependent tumors

Analysis of the gene-protein interaction network in glioma

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