ijms-logo

Journal Browser

Journal Browser

Interplay between Epigenetics and Metabolism in Cancer and Other Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 9319

Special Issue Editor


E-Mail Website
Guest Editor
College of Pharmacy Yonsei Institute of Pharmaceutical Sciences, Yonsei University, Incheon 21983, Republic of Korea
Interests: cancer epigenetics; cancer metabolism; glioblastoma; ovarian cancer; pancreatic cancer; HDAC; KDM; HP1; p53

Special Issue Information

Dear Colleagues,

This Special Issue of International Journal of Molecular Sciences focuses on the interplay between epigenetics and metabolism in physiological and pathological conditions.

Numerous studies have indicated that cellular metabolism and epigenetics are highly interconnected, contributing not only to physiological changes but also to numerous differnt human disorders and cancers. The epigenetic regulation of genes mediated by DNA- and histone-modifying enzymes (DNMT, HAT, HDAC, KAT, KDM, BET, etc.) is influenced by oncogene-mediated metabolic alterations. Such metabolic changes affect the presence or accesibility of cofactors that are required for the catalytic activity of epigenetic modifying enzymes. In addition, these metabolic alterations may produce oncometabolites that abnormally activate or inhibit such modifying enzymes, altering the epigenome. And, vice versa, epigenetic deregulation impacts metabolic gene expression in cancers, resulting in metabolomic alterations. As a result, the interplay between metabolism and epigenetics is crucial for the development of human diseases and tumorigenesis. Discovering novel molecular mechanisms linking the two pathways and targeting their downstream substrates could provide novel therapeutic targets to treat patients with different diseases.

In this issue, we are particularly interested in the regulation and mechanism of epigenetic enzymes and metabolic enzymes in cancer.

We warmly welcome submissions, including original research manuscripts and comprehensive reviews, on this exciting topic.

Dr. So Hee Kwon
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cancer epigenetics
  • cancer metabolism
  • DNMT
  • TET
  • HAT
  • HDAC
  • KMT
  • KDM
  • metabolic enzymes
  • metabolic stress
  • oncometabolites
  • epigenetic enzyme inhibitors
  • cancer metabolism inhibitors

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

17 pages, 1165 KiB  
Review
Glutamine Synthetase as a Therapeutic Target for Cancer Treatment
by Go Woon Kim, Dong Hoon Lee, Yu Hyun Jeon, Jung Yoo, So Yeon Kim, Sang Wu Lee, Ha Young Cho and So Hee Kwon
Int. J. Mol. Sci. 2021, 22(4), 1701; https://doi.org/10.3390/ijms22041701 - 8 Feb 2021
Cited by 34 | Viewed by 8778
Abstract
The significance of glutamine in cancer metabolism has been extensively studied. Cancer cells consume an excessive amount of glutamine to facilitate rapid proliferation. Thus, glutamine depletion occurs in various cancer types, especially in poorly vascularized cancers. This makes glutamine synthetase (GS), the only [...] Read more.
The significance of glutamine in cancer metabolism has been extensively studied. Cancer cells consume an excessive amount of glutamine to facilitate rapid proliferation. Thus, glutamine depletion occurs in various cancer types, especially in poorly vascularized cancers. This makes glutamine synthetase (GS), the only enzyme responsible for de novo synthesizing glutamine, essential in cancer metabolism. In cancer, GS exhibits pro-tumoral features by synthesizing glutamine, supporting nucleotide synthesis. Furthermore, GS is highly expressed in the tumor microenvironment (TME) and provides glutamine to cancer cells, allowing cancer cells to maintain sufficient glutamine level for glutamine catabolism. Glutamine catabolism, the opposite reaction of glutamine synthesis by GS, is well known for supporting cancer cell proliferation via contributing biosynthesis of various essential molecules and energy production. Either glutamine anabolism or catabolism has a critical function in cancer metabolism depending on the complex nature and microenvironment of cancers. In this review, we focus on the role of GS in a variety of cancer types and microenvironments and highlight the mechanism of GS at the transcriptional and post-translational levels. Lastly, we discuss the therapeutic implications of targeting GS in cancer. Full article
Show Figures

Figure 1

Back to TopTop