MYC and tumor metabolism: chicken and egg
Francesca R Dejure,Martin Eilers +1 more
TLDR
The main hypothesis is that regulation of MYC levels is an integral part of the adaptation of cells to nutrient deprivation and that maintaining flexibility of expression is integral to MYC's oncogenic function.Abstract:
Transcription factors of the MYC family are deregulated in the majority of all human cancers. Oncogenic levels of MYC reprogram cellular metabolism, a hallmark of cancer development, to sustain the high rate of proliferation of cancer cells. Conversely, cells need to modulate MYC function according to the availability of nutrients, in order to avoid a metabolic collapse. Here, we review recent evidence that the multiple interactions of MYC with cell metabolism are mutual and review mechanisms that control MYC levels and function in response to metabolic stress situations. The main hypothesis we put forward is that regulation of MYC levels is an integral part of the adaptation of cells to nutrient deprivation. Since such mechanisms would be particularly relevant in tumor cells, we propose that-in contrast to growth factor-dependent controls-they are not disrupted during tumorigenesis and that maintaining flexibility of expression is integral to MYC's oncogenic function.read more
Citations
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The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism.
TL;DR: The role of quercetin in cancer metabolism is discussed, addressing specifically its ability to target molecular pathways involved in glucose metabolism and mitochondrial function.
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PKM2, function and expression and regulation
TL;DR: This paper will use the switching effect of PKM2 in glucose metabolism as the entry point to expand and enrich the Warburg effect, and illustrate the different intracellular localization ofPKM2 and then exert specific biological functions.
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Immunity, Hypoxia, and Metabolism-the Ménage à Trois of Cancer: Implications for Immunotherapy.
Carla Riera-Domingo,Carla Riera-Domingo,Annette Audigé,Sara Granja,Wan-Chen Cheng,Wan-Chen Cheng,Ping-Chih Ho,Ping-Chih Ho,Fátima Baltazar,Christian Stockmann,Massimiliano Mazzone,Massimiliano Mazzone +11 more
TL;DR: This review will discuss how a metabolic characterization of the TME can identify novel targets and signatures that could be exploited in combination with standard immunotherapies and can help to predict the benefit of new and traditional immunotherapeutic drugs.
Journal ArticleDOI
The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis
TL;DR: It is suggested that oncogenic activation of MYC and/or loss of a MYC antagonist, results in an imbalance in the activity of the network as a whole, leading to tumor initiation, progression and maintenance.
Journal ArticleDOI
R-2-hydroxyglutarate attenuates aerobic glycolysis in leukemia by targeting the FTO/m6A/PFKP/LDHB axis.
Ying Qing,Ying Qing,Lei Dong,Lei Gao,Lei Gao,Chenying Li,Chenying Li,Yangchan Li,Yangchan Li,Li Han,Li Han,Emily Prince,Brandon Tan,Xiaolan Deng,Collin Wetzel,Chao Shen,Min Gao,Min Gao,Zhenhua Chen,Wei Li,Bin Zhang,Bin Zhang,Daniel Braas,Johanna ten Hoeve,Gerardo Javier Sanchez,Huiying Chen,Lai N. Chan,Lai N. Chan,Chun-Wei Chen,Chun-Wei Chen,David K. Ann,Lei Jiang,Markus Müschen,Markus Müschen,Markus Müschen,Guido Marcucci,Guido Marcucci,David R. Plas,Zejuan Li,Rui Su,Jianjun Chen,Jianjun Chen +41 more
TL;DR: This paper showed that R-2-hydroxyglutarate (R-2HG) effectively attenuates aerobic glycolysis, a hallmark of cancer metabolism, in (R 2HG-sensitive) leukemia cells, but not in normal CD34+ hematopoietic stem/progenitor cells.
References
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