c-MYC targets the central oscillator gene  Per1  and is regulated by the circadian clock at the post-transcriptional level

Repouskou, Anastasia; Prombona, Anastasia

doi:10.1016/j.bbagrm.2016.02.001

Cited by 31 publications

(32 citation statements)

References 47 publications

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“…In these tumours, MYC expression was associated with elevated Rev-erbα and Odc1 and suppressed Bmal1 (Fig. 2d), while Per2 was suppressed by MYC, consistent with previous findings that MYC can suppress Per expression in some models15.…”

supporting

confidence: 91%

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Correspondence: Oncogenic MYC persistently upregulates the molecular clock component REV-ERBα

et al. 2017

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supporting

confidence: 91%

“…However, the response of other clock genes, such as Per2, to MYC may be context-dependent15. It is also notable that in contrast to Shostak et al .,2 who observed downregulation of REV-ERBα in the presence of ectopic MYC, we previously did not observe downregulation of REV-ERBα in control experiments with activation of MYC-ER Δ106-143 (ref.…”

contrasting

confidence: 74%

Correspondence: Oncogenic MYC persistently upregulates the molecular clock component REV-ERBα

et al. 2017

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“…While whether altered MYC expression in cancer could be mechanistically related to deregulated circadian rhythm either directly or indirectly remains to be established. While E-box elements exist in MYC gene itself [212], MYC and MYC-target genes have been demonstrated to be regulated by CLOCK-BMAL1 at both transcriptional and posttranscriptional levels in mammals [213,214]. Of note, the circadian repressor CRY2 promotes ubiquitylation and degradation of the MYC protein, suggesting that circadian disruption might promote tumorigenesis in part through MYC protein stabilization [215].…”

Section: Myc and The Circadian Clockmentioning

confidence: 99%

WNT signaling and AHCTF1 promote oncogenic MYC expression through super-enhancer-mediated gene gating

et al. 2019

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INTRODUCTION 1.1 EPIGENETIC REGULATION 1.2 CHROMATIN CROSSTALK IN 3D 1.2.1 The innovation of techniques to explore the 3D genome 1.2.2 The genome organizer CTCF and its PARP1 partner 1.2.3 Compartmentalization of nuclear functions in 3D 1.2.4 The active compartments: nuclear interior 1.2.5 The inactive nuclear compartments 1.3 NUCLEOPORINS AND THE GENE GATING PRINCIPLE 1.4 REGULATION OF CIRCADIAN TRANSCRIPTION IN THE COMPARTMENTALIZED NUCLEUS 1.4.1 The central and peripheral clocks 1.4.2 The entrainment of circadian rhythm by external time cues 1.4.3 The clock machinery: driving circadian transcription 1.5 CIRCADIAN CHROMATIN TRANSITIONS 1.5.1 The establishment of active chromatin states by the positive limb 1.5.2 The establishment of repressed chromatin states by the negative limb 1.5.3 Crosstalk between the positive and negative limb of the clock machinery during chromatin transitions 1.6 CIRCADIAN CLOCK, CELLULAR METABOLISM AND COMPLEX DISEASES 2 AIMS 3 METHODS AND MATERIALS 3.1 CELL CULTURES AND TREATMENTS 3.2 RNA/DNA FISH ANALYSES 3.3 IN SITU PROXIMITY LIGATION ASSAY (ISPLA) 3.4 CHROMATIN IN SITU PROXIMITY (CHRISP) 3.5 GRID WIDE-FIELD MICROSCOPY 3.6 CHROMATIN NETWORKS AND INTEGRATION ANALYSES 3.6.1 Circular chromatin conformation capture sequencing (4C-Seq) 3.6.2 Nodewalk 3.7 RNA ANLYSES 3.7.1 Pulse labeling of RNA 3.7.2 The nuclear RNA export assay 3.7.3 mRNA decay analyses 3.7.4 RT-QPCR analysis of transcription 4 RESULTS 4.1 PAPER I: PARP1-AND CTCF-MEDIATED INTERACTIONS BETWEEN ACTIVE AND REPRESSED CHROMATIN AT THE LAMINA PROMOTE OSCILLATING TRANSCRIPTION 4.1.1 Interactome connecting circadian loci and LADs 4.1.2 Molecular ties connecting circadian loci to LADs 4.1.3 The role of the nuclear periphery in circadian transcriptional attenuation 4.1.4 Summary: novel principles in the entrainment of circadian transcription 6 4.2 PAPER II: WNT SIGNALING AND AHCTF1 PROMOTE ONCOGENIC MYC EXPRESSION THROUGH SUPER-ENHANCER-MEDIATED GENE GATING 4.2.1 Regulation of MYC transcription in 3D 4.2.2 Contribution of gene gating to MYC mRNA accumulation 4.2.3 The role of WNT in the super-enhancer mediated gene gating of MYC 5 DISCUSSIONS 5.1 THE ROLE OF NUCLEAR PERIPHERY IN THE REGULATION OF GENE EXPRESSION 5.2 MYC AND THE CIRCADIAN CLOCK 5.3 ADAPTATION TO THE ENVIRONMENT 5.3.1 WNT signaling 5.3.2 Circadian entrainment 5.3.3 Nucleoporins and the transcriptional memory 5.4 CTCF AND PARP1 IN COMPLEX DISEASES 5.4.

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“…c-MYC expression can be regulated by E-boxes in its own promoter and by core clock proteins (74, 75). Additionally, it can also be regulated at the posttranslational level (76), with a very recent study indicating that the circadian repressor protein CRY2 targets MYC for degradation via the F-box protein FBXW7 (77). Thus, a negative cross talk between the MYC pathway and circadian oscillator is likely to exist in cancer cells.…”

Section: Myc—a Potential Link Between Hematological Malignancies and mentioning

confidence: 99%

Desynchronization of Circadian Clocks in Cancer: A Metabolic and Epigenetic Connection

Padmanabhan

Billaud

2017

Front. Endocrinol.

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Circadian clocks are innate oscillators that drive daily rhythms in metabolism, physiology, and behavior. 24-h rhythms in gene expression, driven by core clock transcription factors, reflect the epigenetic state of the cell, which in turn is dictated by the metabolic environment. Cancer cells alter their metabolic state and gene expression and therefore are likely to tweak circadian clock function in their favor. Over the past decade, we have witnessed an extraordinary increase in systems-level studies that suggest intricate mechanistic links between the cellular metabolome and the circadian epigenome. In parallel, reprogramming of cellular clock function in cancers is increasingly evident and the role of clock genes in the development of hematological tumors, as well as their pathophysiological effects on tissues distal to the tumor, has been described. Furthermore, the interplay between components of the circadian clock, metabolic enzymes, and oncogenes is starting to be better understood, such as the close association between overexpression of the Myc oncogene and perturbation of circadian and metabolic rhythms, thus opening new avenues to treat cancers. This review article explores current knowledge on the circadian metabolome and the molecular pathways they control, with a focus on their involvement in the development of hematopoietic malignancies.

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c-MYC targets the central oscillator gene Per1 and is regulated by the circadian clock at the post-transcriptional level

Cited by 31 publications

References 47 publications

Correspondence: Oncogenic MYC persistently upregulates the molecular clock component REV-ERBα

Correspondence: Oncogenic MYC persistently upregulates the molecular clock component REV-ERBα

WNT signaling and AHCTF1 promote oncogenic MYC expression through super-enhancer-mediated gene gating

Desynchronization of Circadian Clocks in Cancer: A Metabolic and Epigenetic Connection

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