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

Altman, Brian J.; Hsieh, Annie L.; Gouw, Arvin M.; Dang, Chi V.

doi:10.1038/ncomms14862

Cited by 18 publications

(34 citation statements)

References 15 publications

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“…Disruption of the molecular clock is associated with a variety of human pathologies, including cancer [6,21]. Ectopic overexpression of the oncogenic MYC protein has been recently reported to alter circadian gene expression in cancer cell lines, although the molecular mechanism behind this MYC function is still highly debated [22][23][24][25].…”

Section: Introductionmentioning

confidence: 99%

MYC-Associated Factor MAX is a Regulator of the Circadian Clock

Blaževitš

Bolshette

Vecchio

et al. 2020

IJMS

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The circadian transcriptional network is based on a competition between transcriptional activator and repressor complexes regulating the rhythmic expression of clock-controlled genes. We show here that the MYC-associated factor X, MAX, plays a repressive role in this network and operates through a MYC-independent binding to E-box-containing regulatory regions within the promoters of circadian BMAL1 targets. We further show that this “clock” function of MAX is required for maintaining a proper circadian rhythm and that MAX and BMAL1 contribute to two temporally alternating transcriptional complexes on clock-regulated promoters. We also identified MAX network transcriptional repressor, MNT, as a fundamental partner of MAX-mediated circadian regulation. Collectively, our data indicate that MAX regulates clock gene expression and contributes to keeping the balance between positive and negative elements of the molecular clock machinery.

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Section: Introductionmentioning

confidence: 99%

MYC-Associated Factor MAX is a Regulator of the Circadian Clock

Blaževitš

Bolshette

Vecchio

et al. 2020

IJMS

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“…These normal pathways are under tight control of feed-back loops that return cells to a resting state when nutrients and growth signals are insufficient. Emerging evidence has shown oncogenic disruption of the clock in cancer cells [83-85]. This presents the possibility that metabolic toxicity to normal tissues could be spared and efficacy against cancer cells increased by taking the circadian clock into consideration.…”

Section: Discussionmentioning

confidence: 99%

Exploiting Metabolic Vulnerabilities of Cancer with Precision and Accuracy

Wolpaw

Dang

2018

Trends in Cell Biology

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108

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Links between oncogenic drivers and cancer cell metabolism have emerged over the past several decades, indicating that constitutive oncogenic growth signaling can render cancers susceptible to metabolic interventions. While significant progress has been achieved in the identification of metabolic vulnerabilities of cancer cells, the complexity of the tumor microenvironment (TME) and the dynamic nature of organismal circadian metabolism challenge the precision of targeting cancer metabolism. Here current progress in the areas of cancer metabolism and TME metabolism is reviewed, highlighting how cancer metabolism can be accurately and precisely targeted.

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“…This activity of MYC was initially reported to be dependent on the negative transcriptional arm of the clock through REV-ERBα that inhibits expression of Bmal1 and also deregulates oscillations in metabolic sensing through AMPK and hexokinases HK1 and HK2 [68]. Recent evidence also suggests that MYC-dependent activity may not be solely dependent on REV-ERBα [69, 70]. The nutrient-sensing function of the MYC superfamily plays an important role in tumor metabolism (Figure 3).…”

Section: Linking the Clock Metabolism And Cancermentioning

confidence: 99%

Circadian Clocks and Cancer: Timekeeping Governs Cellular Metabolism

Verlande

Masri

2019

Trends in Endocrinology & Metabolism

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The circadian clock is a biological mechanism that dictates an array of rhythmic physiological processes. Virtually all cells contain a functional clock whose disruption results in altered timekeeping and detrimental systemic effects, including cancer. Recent advances have connected genetic disruption of the clock with multiple transcriptional and signaling networks controlling tumor initiation and progression. An additional feature of this circadian control relies on cellular metabolism both within the tumor microenvironment and the organism systemically. A discussion of major advances related to cancer metabolism and the circadian clock will be outlined, including new efforts related to metabolic flux of transformed cells, metabolic heterogeneity of tumors, and the implications of circadian control of these pathways.

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

Cited by 18 publications

References 15 publications

MYC-Associated Factor MAX is a Regulator of the Circadian Clock

MYC-Associated Factor MAX is a Regulator of the Circadian Clock

Exploiting Metabolic Vulnerabilities of Cancer with Precision and Accuracy

Circadian Clocks and Cancer: Timekeeping Governs Cellular Metabolism

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