Cell cycle transcription control: DREAM/MuvB and RB-E2F complexes

Fischer, Martin; Müller, G

doi:10.1080/10409238.2017.1360836

Cited by 199 publications

(276 citation statements)

References 306 publications

(369 reference statements)

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“…37 E2F promoter sites have been linked to transcriptional repression in resting cells and activation during the cell cycle. 38 Further study showed that heavy-ion irradiation could induce p53 cancer cell apoptosis through the E2F1 signal pathway. p53 is crucial in multicellular organisms, because it prevents cancer formation and consequently functions as a tumor suppressor.…”

Section: Discussionmentioning

confidence: 99%

“…The E2F family plays an important role in the process, acting as a protein, and is associated with both cell proliferation and ‐dependent . E2F promoter sites have been linked to transcriptional repression in resting cells and activation during the cell cycle . Further study showed that heavy‐ion irradiation could induce p53 cancer cell apoptosis through the E2F1 signal pathway.…”

Section: Discussionmentioning

confidence: 99%

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Differential protein‐coding gene and long noncoding RNA expression in smoking‐related lung squamous cell carcinoma

Sun

Miao

et al. 2017

Thoracic Cancer

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BackgroundCigarette smoking is one of the greatest preventable risk factors for developing cancer, and most cases of lung squamous cell carcinoma (lung SCC) are associated with smoking. The pathogenesis mechanism of tumor progress is unclear. This study aimed to identify biomarkers in smoking‐related lung cancer, including protein‐coding gene, long noncoding RNA, and transcription factors.MethodsWe selected and obtained messenger RNA microarray datasets and clinical data from the Gene Expression Omnibus database to identify gene expression altered by cigarette smoking. Integrated bioinformatic analysis was used to clarify biological functions of the identified genes, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, the construction of a protein–protein interaction network, transcription factor, and statistical analyses. Subsequent quantitative real‐time PCR was utilized to verify these bioinformatic analyses.ResultsFive hundred and ninety‐eight differentially expressed genes and 21 long noncoding RNA were identified in smoking‐related lung SCC. GO and KEGG pathway analysis showed that identified genes were enriched in the cancer‐related functions and pathways. The protein–protein interaction network revealed seven hub genes identified in lung SCC. Several transcription factors and their binding sites were predicted. The results of real‐time quantitative PCR revealed that AURKA and BIRC5 were significantly upregulated and LINC00094 was downregulated in the tumor tissues of smoking patients. Further statistical analysis indicated that dysregulation of AURKA, BIRC5, and LINC00094 indicated poor prognosis in lung SCC.ConclusionProtein‐coding genes AURKA, BIRC5, and LINC00094 could be biomarkers or therapeutic targets for smoking‐related lung SCC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Differential protein‐coding gene and long noncoding RNA expression in smoking‐related lung squamous cell carcinoma

Sun

Miao

et al. 2017

Thoracic Cancer

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“…One of the genes with increased accessibility and expression in SP cells was E2F3 , an E2F family member, which plays a key role in cell cycle control. E2F s are normally sequestered via Rb1 binding, but in late G1 phase Rb1 becomes multiphosphorylated by cyclin‐dependent kinases and liberates E2F , which in turn binds E2F recognition sites at genes required for DNA synthesis and replication and recruits Pol II and acetyltransferases to activate transcription . In addition to promoting S phase, E2F3 has been shown to interact with a complex network of miRNAs in various malignancies, creating feedback loops that modulate proliferation, invasion, apoptosis and metastasis .…”

Section: Discussionmentioning

confidence: 99%

Epigenetic plasticity potentiates a rapid cyclical shift to and from an aggressive cancer phenotype

Wei

et al. 2020

Intl Journal of Cancer

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Highly tumorigenic, drug‐resistant cancer stem‐like cells drive cancer progression. These aggressive cells can arise repeatedly from bulk tumor cells independently of mutational events, suggesting an epigenetic mechanism. To test this possibility, we studied bladder cancer cells as they cyclically shifted to and from a cancer stem‐like phenotype, and we discovered that these two states exhibit distinct DNA methylation and chromatin accessibility. Most differential chromatin accessibility was independent of methylation and affected the expression of driver genes such as E2F3, a cell cycle regulator associated with aggressive bladder cancer. Cancer stem‐like cells exhibited increased E2F3 promoter accessibility and increased E2F3 expression that drove cell migration, invasiveness and drug resistance. Epigenetic interference using a DNA methylation inhibitor blocked the transition to a cancer stem‐like state and reduced E2F3 expression. Our findings indicate that epigenetic plasticity plays a key role in the transition to and from an aggressive, drug‐resistant phenotype.

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“…1,11 Indels or other genetic alterations were not found in RB1, frequently mutated in NUP98-KDM5A AMKL. 11 According to RNAseq data, the expression profile of RB1 and G1/S cell cycle genes regulated by RB-E2F complexes 12 was broadly similar in AMKL and CB-CD34 1 cells (Supporting Information Figure S1).…”

Section: Ca S E Re P O Rtmentioning

confidence: 99%

NUP98‐BPTF gene fusion identified in primary refractory acute megakaryoblastic leukemia of infancy

Roussy

Bilodeau

Jouan

et al. 2018

Genes Chromosomes & Cancer

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The advent of large scale genomic sequencing technologies significantly improved the molecular classification of acute megakaryoblastic leukaemia (AMKL). AMKL represents a subset (∼10%) of high fatality pediatric acute myeloid leukemia (AML). Recurrent and mutually exclusive chimeric gene fusions associated with pediatric AMKL are found in 60%-70% of cases and include RBM15-MKL1, CBFA2T3-GLIS2, NUP98-KDM5A and MLL rearrangements. In addition, another 4% of AMKL harbor NUP98 rearrangements (NUP98r), with yet undetermined fusion partners. We report a novel NUP98-BPTF fusion in an infant presenting with primary refractory AMKL. In this NUP98r, the C-terminal chromatin recognition modules of BPTF, a core subunit of the NURF (nucleosome remodeling factor) ATP-dependent chromatin-remodeling complex, are fused to the N-terminal moiety of NUP98, creating an in frame NUP98-BPTF fusion, with structural homology to NUP98-KDM5A. The leukemic blasts expressed two NUP98-BPTF splicing variants, containing one or two tandemly spaced PHD chromatin reader domains. Our study also identified an unreported wild type BPTF splicing variant encoding for 2 PHD domains, detected both in normal cord blood CD34 cells and in leukemic blasts, as with the fly BPTF homolog, Nurf301. Disease course was marked by rapid progression and primary chemoresistance, with ultimately significant tumor burden reduction following treatment with a clofarabine containing regimen. In sum, we report 2 novel NUP98-BPTF fusion isoforms that contribute to refine the NUP98r subgroup of pediatric AMKL. Multicenter clinical trials are critically required to determine the frequency of this fusion in AMKL patients and explore innovative treatment strategies for a disease still plagued with poor outcomes.

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Cell cycle transcription control: DREAM/MuvB and RB-E2F complexes

Cited by 199 publications

References 306 publications

Differential protein‐coding gene and long noncoding RNA expression in smoking‐related lung squamous cell carcinoma

Differential protein‐coding gene and long noncoding RNA expression in smoking‐related lung squamous cell carcinoma

Epigenetic plasticity potentiates a rapid cyclical shift to and from an aggressive cancer phenotype

NUP98‐BPTF gene fusion identified in primary refractory acute megakaryoblastic leukemia of infancy

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