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Signaling and Gene Regulation in Metabolism
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Signaling and Gene Regulation in Metabolism

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (25 October 2023) | Viewed by 8133

Special Issue Editors

Prof. Dr. Estela Jacinto

E-Mail Website
Guest Editor
Department of Biochemistry & Molecular Biology, Rutgers Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA
Interests: signal transduction; cancer; insulin; metabolism; T lymphocytes
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Mei Kong

E-Mail Website
Guest Editor
School of Biological Sciences, University of California, Irvine 3219 McGaugh Hall, Irvine, CA 92697, USA
Interests: nutritional microenvironment in tumor development and drug response; metabolism and epigenetics; protein phosphatase regulation in diabetes and obesity

Special Issue Information

Dear Colleagues,

Nutrient metabolism generates fuel and biosynthetic precursors necessary for cellular and organismal growth. The consumption and metabolism of nutrients are controlled by signaling pathways that respond to fluctuations in nutrient levels. These signaling pathways also integrate other environmental inputs including the presence of growth signals and stress stimuli. The transduction of signals from the cellular membrane to the nucleus leads to regulation of gene expression, which ultimately allows cells to establish metabolic homeostasis, which is necessary to prevent disease. Understanding how signaling and changes in gene expression reprogram metabolism and how defects in these processes lead to pathological conditions will facilitate the development of better therapeutic strategies against metabolism-related disorders. The mTOR and AMPK signaling pathways control a variety of metabolic effectors but the role of other signaling molecules also deserve further investigation. This Special Issue aims to gather new insights on how different signaling pathways control various metabolic processes. Other topics of relevance to this Special Issue also include: how various types of nutrients or metabolites are sensed, modulation of nutrient uptake and metabolism, coordinated regulation of metabolic processes, and transcriptional and epigenetic control of metabolic processes. We will also highlight underlying mechanisms, therapeutic strategies and dietary manipulations involving metabolic-related disorders.

Prof. Dr. Estela Jacinto
Prof. Dr. Mei Kong
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metabolism
  • signaling to metabolism
  • regulation of metabolic pathways
  • nutrients
  • dietary manipulations in cancer and other metabolic disorders
  • mTOR/AMPK pathways
  • insulin/PI3K signaling
  • cell growth and proliferation

Published Papers (2 papers)

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Research

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15 pages, 2756 KiB  
Article
Alpha-Ketoglutarate Regulates Tnfrsf12a/Fn14 Expression via Histone Modification and Prevents Cancer-Induced Cachexia
by Bryan I. Ruiz, Xazmin H. Lowman, Ying Yang, Qi Fan, Tianhong Wang, Hongmei Wu, Eric A. Hanse and Mei Kong
Genes 2023, 14(9), 1818; https://0-doi-org.brum.beds.ac.uk/10.3390/genes14091818 - 19 Sep 2023
Cited by 1 | Viewed by 1686
Abstract
Previous studies have shown that inhibition of TNF family member FN14 (gene: TNFRSF12A) in colon tumors decreases inflammatory cytokine expression and mitigates cancer-induced cachexia. However, the molecular mechanisms underlying the regulation of FN14 expression remain unclear. Tumor microenvironments are often devoid of [...] Read more.
Previous studies have shown that inhibition of TNF family member FN14 (gene: TNFRSF12A) in colon tumors decreases inflammatory cytokine expression and mitigates cancer-induced cachexia. However, the molecular mechanisms underlying the regulation of FN14 expression remain unclear. Tumor microenvironments are often devoid of nutrients and oxygen, yet how the cachexic response relates to the tumor microenvironment and, importantly, nutrient stress is unknown. Here, we looked at the connections between metabolic stress and FN14 expression. We found that TNFRSF12A expression was transcriptionally induced during glutamine deprivation in cancer cell lines. We also show that the downstream glutaminolysis metabolite, alpha-ketoglutarate (aKG), is sufficient to rescue glutamine-deprivation-promoted TNFRSF12A induction. As aKG is a co-factor for histone de-methylase, we looked at histone methylation and found that histone H3K4me3 at the Tnfrsf12a promoter is increased under glutamine-deprived conditions and rescued via DM-aKG supplementation. Finally, expression of Tnfrsf12a and cachexia-induced weight loss can be inhibited in vivo by DM-aKG in a mouse cancer cachexia model. These findings highlight a connection between metabolic stress and cancer cachexia development. Full article
(This article belongs to the Special Issue Signaling and Gene Regulation in Metabolism)
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Review

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42 pages, 3406 KiB  
Review
The Hexosamine Biosynthesis Pathway: Regulation and Function
by Alysta Paneque, Harvey Fortus, Julia Zheng, Guy Werlen and Estela Jacinto
Genes 2023, 14(4), 933; https://0-doi-org.brum.beds.ac.uk/10.3390/genes14040933 - 18 Apr 2023
Cited by 24 | Viewed by 5862
Abstract
The hexosamine biosynthesis pathway (HBP) produces uridine diphosphate-N-acetyl glucosamine, UDP-GlcNAc, which is a key metabolite that is used for N- or O-linked glycosylation, a co- or post-translational modification, respectively, that modulates protein activity and expression. The production of hexosamines [...] Read more.
The hexosamine biosynthesis pathway (HBP) produces uridine diphosphate-N-acetyl glucosamine, UDP-GlcNAc, which is a key metabolite that is used for N- or O-linked glycosylation, a co- or post-translational modification, respectively, that modulates protein activity and expression. The production of hexosamines can occur via de novo or salvage mechanisms that are catalyzed by metabolic enzymes. Nutrients including glutamine, glucose, acetyl-CoA, and UTP are utilized by the HBP. Together with availability of these nutrients, signaling molecules that respond to environmental signals, such as mTOR, AMPK, and stress-regulated transcription factors, modulate the HBP. This review discusses the regulation of GFAT, the key enzyme of the de novo HBP, as well as other metabolic enzymes that catalyze the reactions to produce UDP-GlcNAc. We also examine the contribution of the salvage mechanisms in the HBP and how dietary supplementation of the salvage metabolites glucosamine and N-acetylglucosamine could reprogram metabolism and have therapeutic potential. We elaborate on how UDP-GlcNAc is utilized for N-glycosylation of membrane and secretory proteins and how the HBP is reprogrammed during nutrient fluctuations to maintain proteostasis. We also consider how O-GlcNAcylation is coupled to nutrient availability and how this modification modulates cell signaling. We summarize how deregulation of protein N-glycosylation and O-GlcNAcylation can lead to diseases including cancer, diabetes, immunodeficiencies, and congenital disorders of glycosylation. We review the current pharmacological strategies to inhibit GFAT and other enzymes involved in the HBP or glycosylation and how engineered prodrugs could have better therapeutic efficacy for the treatment of diseases related to HBP deregulation. Full article
(This article belongs to the Special Issue Signaling and Gene Regulation in Metabolism)
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