Epigenetic Reprogramming of the Glucose Metabolic Pathways by the Chromatin Effectors During Cancer

Mondal, Payel; Tiwary, Niharika; Sengupta, Aditi; Dhang, Sinjini; Roy, Siddhartha; Das, Chandrima

doi:10.1007/978-3-031-07634-3_9

Cited by 2 publications

(4 citation statements)

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“…Once phosphorylated at Ser10 or Ser28, there is recruitment of 14-3-3ε and ζ, readers of the phosphorylated mark (Winter et al 2008;Drobic et al 2010). In addition to the phospho-Ser readers are proteins binding to the acetyl Lys and other modified amino acids (Mondal et al 2022). How do these readers function together to induce transcription initiated by MSK1/2?…”

Section: Discussionmentioning

confidence: 99%

Mitogen- and stress-activated protein kinase (MSK1/2) regulated gene expression in normal and disease states

Sattarifard

Safaei

Khazeeva

et al. 2023

Biochem. Cell Biol.

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The mitogen- and stress-activated protein kinases (MSK) are epigenetic modifiers that regulate gene expression in normal and disease cell states. MSK1 and 2 are involved in a chain of signal transduction events bringing signals from the external environment of a cell to specific sites in the genome. MSK1/2 phosphorylate histone H3 at multiple sites, resulting in chromatin remodeling at regulatory elements of target genes and the induction of gene expression. Several transcription factors (RELA of NF-κB, CREB) are also phosphorylated by MSK1/2 and contribute to induction of gene expression. In response to signal transduction pathways, MSK1/2 can stimulate genes involved in cell proliferation, inflammation, innate immunity, neuronal function, and neoplastic transformation. Abrogation of the MSK-involved signaling pathway is among the mechanisms by which pathogenic bacteria subdue the host’s innate immunity. Depending on the signal transduction pathways in play and the MSK-targeted genes, MSK may promote or hinder metastasis. Thus, depending on the type of cancer and genes involved, MSK overexpression may be a good or poor prognostic factor. In this review, we focus on mechanisms by which MSK1/2 regulate gene expression, and recent studies on their roles in normal and diseased cells.

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Section: Discussionmentioning

confidence: 99%

Mitogen- and stress-activated protein kinase (MSK1/2) regulated gene expression in normal and disease states

Sattarifard

Safaei

Khazeeva

et al. 2023

Biochem. Cell Biol.

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“…This, therefore, intimately couples cellular metabolic and epigenomic states owing to the shared generation and use of cofactors and metabolites. As such, a cell’s metabolic state can drastically shape and alter its epigenetic state and epigenetic alterations can propagate and alter a cell’s metabolic state [ 451 , 452 , 453 , 454 ].…”

Section: Epigenetics and Epigenomementioning

confidence: 99%

“…Through these TET-mediated oxidation reactions, a cell is able to actively and/or passively demethylate DNA [ 485 , 519 ]. It is pertinent to note that the intermediates and cofactors of these successive reactions are derived from other cellular processes, primarily metabolism [ 451 , 452 , 453 , 454 ]. Intermediates such as α-KG, O 2 , CO 2 , succinate, fumarate, and 2-HG are all metabolic factors [ 451 , 452 , 453 , 454 ].…”

Section: Dna Methylationmentioning

confidence: 99%

“…It is pertinent to note that the intermediates and cofactors of these successive reactions are derived from other cellular processes, primarily metabolism [ 451 , 452 , 453 , 454 ]. Intermediates such as α-KG, O 2 , CO 2 , succinate, fumarate, and 2-HG are all metabolic factors [ 451 , 452 , 453 , 454 ]. As such, perturbations to the availability and concentration of these intermediates either through metabolic regulation, metabolic inhibition, diet, or environmental factors will affect a cell’s ability to regulate methylation adequately.…”

Section: Dna Methylationmentioning

confidence: 99%

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The Interplay between Dysregulated Metabolism and Epigenetics in Cancer

Bassal

2023

Biomolecules

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Cellular metabolism (or energetics) and epigenetics are tightly coupled cellular processes. It is arguable that of all the described cancer hallmarks, dysregulated cellular energetics and epigenetics are the most tightly coregulated. Cellular metabolic states regulate and drive epigenetic changes while also being capable of influencing, if not driving, epigenetic reprogramming. Conversely, epigenetic changes can drive altered and compensatory metabolic states. Cancer cells meticulously modify and control each of these two linked cellular processes in order to maintain their tumorigenic potential and capacity. This review aims to explore the interplay between these two processes and discuss how each affects the other, driving and enhancing tumorigenic states in certain contexts.

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Epigenetic Reprogramming of the Glucose Metabolic Pathways by the Chromatin Effectors During Cancer

Cited by 2 publications

References 269 publications

Mitogen- and stress-activated protein kinase (MSK1/2) regulated gene expression in normal and disease states

Mitogen- and stress-activated protein kinase (MSK1/2) regulated gene expression in normal and disease states

The Interplay between Dysregulated Metabolism and Epigenetics in Cancer

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