MEF Promotes Stemness in the Pathogenesis of Gliomas

Bazzoli, Elena; Pulvirenti, Teodoro; Oberstadt, Moritz C.; Perna, Fabiana; Wee, Boyoung; Schultz, Nikolaus; Huse, Jason T.; Fomchenko, Elena I.; Voza, Francesca; Tabar, Viviane; Brennan, Cameron; DeAngelis, Lisa M.; Nimer, Stephen D.; Holland, Eric C.; Squatrito, Massimo

doi:10.1016/j.stem.2012.09.012

Cited by 38 publications

(45 citation statements)

References 32 publications

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“…2C) and was generated by an intrachromosomal inversion (27). ELF4/ myeloid elf-1 like factor (MEF) is a transcriptional activator that regulates hematopoietic and glioma stem cell functions as well as several lymphocytes and myelocytes (28,29). As a consequence of the chimeric fusion protein, BCORL1-ELF4 exhibited decreased repression activity compared with BCORL1 (27).…”

Section: Bcorl1-e74-like Factor 4 Fusion In Hepatocellular Carcinomamentioning

confidence: 99%

Clarifying the Impact of Polycomb Complex Component Disruption in Human Cancers

Yamamoto

Abe

Emi

2014

Molecular Cancer Research

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The dysregulation of proper transcriptional control is a major cause of developmental diseases and cancers. Polycomb proteins form chromatin-modifying complexes that transcriptionally silence genome regions in higher eukaryotes. The BCL6 corepressor (BCOR) complex comprises ring finger protein 1B (RNF2/RING1B), polycomb group ring finger 1 (PCGF1), and lysine-specific demethylase 2B (KDM2B) and is uniquely recruited to nonmethylated CpG islands, where it removes histone H3K36me2 and induces repressive histone H2A monoubiquitylation. Germline BCOR mutations have been detected in patients with oculofaciocardiodental and Lenz microphthalmia syndromes, which are inherited conditions. Recently, several variants of BCOR and BCORlike 1 (BCORL1) chimeric fusion transcripts were reported in human cancers, including acute promyelocytic leukemia, bone sarcoma, and hepatocellular carcinoma. In addition, massively parallel sequencing has identified inactivating somatic BCOR and BCORL1 mutations in patients with acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), chronic myelomonocytic leukemia, medulloblastoma, and retinoblastoma. More importantly, patients with AML and MDS with BCOR mutations exhibit poor prognosis. This perspective highlights the detection of BCOR mutations and fusion transcripts of BCOR and BCORL1 and discusses their importance for diagnosing cancer subtypes and estimating the treatment responses of patients. Furthermore, this perspective proposes the need for additional functional studies to clarify the oncogenic mechanism by which BCOR and BCORL1 are disrupted in cancers, and how this may lead to the development of novel therapeutics. Mol Cancer Res; 12(4); 479-84. Ó2014 AACR. IntroductionA major cause of developmental diseases and cancers is the dysregulation of proper transcriptional control, a process that is directly regulated by transcription factors, coactivators, and corepressors. Till date, several hundred transcriptional coregulators have been reported in the literature. Recently, the increased use of massively parallel sequencing techniques has expanded our knowledge on the induction of congenital diseases and cancers caused by specific gene mutations.

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Section: Bcorl1-e74-like Factor 4 Fusion In Hepatocellular Carcinomamentioning

confidence: 99%

Clarifying the Impact of Polycomb Complex Component Disruption in Human Cancers

Yamamoto

Abe

Emi

2014

Molecular Cancer Research

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“…ELF4 regulates hematopoietic stem cell quiescence and self-renewal (Lacorazza et al, 2006;Liu et al, 2009). ELF4 also regulates self-renewal of braintumor stem cells (Bazzoli et al, 2012). In addition, ELF4 plays an important role in osteogenic differentiation and bone development (Kim et al, 2007;Seul et al, 2011;Baek et al, 2012).…”

Section: Elf4 (E74-like Factor 4 (Ets Domain Transcription Factor))mentioning

confidence: 99%

“…The acquisition of stem-like traits might contribute to glioma initiation, growth, and recurrence. ELF4 is highly expressed in both human and mouse glioblastomas and its absence impairs gliomagenesis in a PDGF-driven glioma mouse model (Bazzoli et al, 2012). Prognosis High levels of ELF4 expression in gliomas are associated with a poor prognosis (Bazzoli et al, 2012).…”

Section: Gliomasmentioning

confidence: 99%

“…ELF4 is highly expressed in both human and mouse glioblastomas and its absence impairs gliomagenesis in a PDGF-driven glioma mouse model (Bazzoli et al, 2012). Prognosis High levels of ELF4 expression in gliomas are associated with a poor prognosis (Bazzoli et al, 2012). Oncogenesis Modulation of ELF4 levels in both mouse neural stem cells and human glioblastoma cells has a significant impact on neurosphere formation.…”

Section: Gliomasmentioning

confidence: 99%

“…Oncogenesis Modulation of ELF4 levels in both mouse neural stem cells and human glioblastoma cells has a significant impact on neurosphere formation. Thus, ELF4 is a gatekeeper gene that promotes stemness in the pathogenesis of gliomas (Bazzoli et al, 2012).…”

Section: Gliomasmentioning

confidence: 99%

See 2 more Smart Citations

ELF4 (E74-like factor 4 (ets domain transcription factor))

Nimer¹,

Liu²

2014

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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Functional characterization of the Sox2, c‐Myc, and Oct4 promoters

Chen

Jin

Song

et al. 2018

J of Cellular Biochemistry

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To better understand the mechanisms in transcriptional regulation, we analyzed the promoters of the reprogramming key genes Sox2, c‐Myc, and Oct4. Here, we cloned different 5′ deletions of the goat Sox2, c‐Myc, and Oct4 promoters, and evaluated their functions by green fluorescent protein reporter system and dual‐luciferase reporter system. Site‐directed mugagenesis and epigenetic modifiers were used to explore the influence of transcription binding sites and epigenetic status on the promoters. The results suggested that the basal promoters were located in the − 109 to 49, − 147 to 1, and − 96 to 30 bp regions of the Sox2, c‐Myc, and Oct4 promoters. The transcription factors that identified to influence the Sox2, c‐Myc, and Oct4 promoter activities were Elf‐1 and activating protein 2 (AP‐2), C/EBP and Sp1, and Mzf1 and Sp1, respectively. The epigenetic alternation of the Sox2, c‐Myc, and Oct4 promoters by 5‐aza‐2′‐deoxycytidine or/and trichostatin A significantly increased the promoter activities. In conclusion, the result determined the core promoter areas of the Sox2, c‐Myc, and Oct4 genes, and identified the transcription factors that influence their promoter activities. We also verified that the Sox2, c‐Myc, and Oct4 promoters were hypermethylated and hypoacetylated.

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MEF Promotes Stemness in the Pathogenesis of Gliomas

Cited by 38 publications

References 32 publications

Clarifying the Impact of Polycomb Complex Component Disruption in Human Cancers

Clarifying the Impact of Polycomb Complex Component Disruption in Human Cancers

ELF4 (E74-like factor 4 (ets domain transcription factor))

Functional characterization of the Sox2, c‐Myc, and Oct4 promoters

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