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New Aspects of Bioenergetics in Cancer
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New Aspects of Bioenergetics in Cancer

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

Deadline for manuscript submissions: 20 June 2025 | Viewed by 2032

Special Issue Editor

Dr. Yunfeng Zhao

E-Mail Website
Guest Editor
Department of Pharmacology, Toxicology & Neuroscience, LSU Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA
Interests: carcinogenesis; oxidative stress; toxicology; cancer metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Dysregulating cellular metabolism is one of the hallmarks of cancer, and cancer bioenergetics is a critical portion of cancer metabolism, playing an important role in ATP production, biosynthesis and redox balance in cancer cells. Cancer bioenergetics include, but are not limited to, the following topics:

  • Mutational activation of metabolic enzymes in cancer;
  • Epigenetic regulation of cancer biogenetics;
  • Biogenetics regulated by oncogenes/tumor suppressor genes; 
  • Kinases/phosphatases in cancer biogenetics;
  • Membrane transporters in cancer metabolism;
  • New concepts in cancer bioenergetics;
  • New tools to study cancer biogenetics;
  • Other topics in cancer metabolism.

Dr. Yunfeng Zhao
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 metabolism
  • bioenergetics
  • mitochondria
  • redox

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Published Papers (1 paper)

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Research

13 pages, 3486 KiB  
Article
NAD+ Boosting Through NRH Supplementation Enhances Treatment Efficacy in EOC In Vitro
by Kevin J. Lee, Sagar Chokshi, Tanvi Joshi, Mackenzie Cummings, Catherine E. Lyons, Mary Howard Singleton, Elizabeth Catranis, Luciana Madiera da Silva, Faisal Hayat, Marie Migaud and Jennifer Scalici
Int. J. Mol. Sci. 2025, 26(4), 1719; https://doi.org/10.3390/ijms26041719 - 18 Feb 2025
Viewed by 1331
Abstract
Dihydronicotinamide rioside (NRH), the reduced form of nicotinamide riboside (NR), is a recently identified, naturally occurring precursor of arguably the most crucial cofactor for cellular function, nicotinamide adenine dinucleotide (NAD+). Recent investigation suggests that NRH is more adept at increasing NAD+ stores than [...] Read more.
Dihydronicotinamide rioside (NRH), the reduced form of nicotinamide riboside (NR), is a recently identified, naturally occurring precursor of arguably the most crucial cofactor for cellular function, nicotinamide adenine dinucleotide (NAD+). Recent investigation suggests that NRH is more adept at increasing NAD+ stores than traditional NAD+ precursors, and such extreme NAD+ boosting via NRH supplementation induces cytotoxicity in certain cellular contexts. It has also been shown that the lack of functional BRCA protein in epithelial ovarian cancer (EOC) directly impacts intracellular NAD+ levels. Given that altered cellular metabolism and DNA repair mechanisms are central alterations in EOC, and these processes are functionally dependent on NAD+, we sought to assess whether NRH supplementation in EOC cell lines enhanced cellular cytotoxicity alone and in combination with standard therapeutic agents. Significant cytotoxicity was noted in NRH treated cells (~40%) with minimal cell death in the nicotinic acid (NA)-treated lines. Levels of NAD(P)H were confirmed to have increased with NRH supplementation, albeit at different levels among the different cell lines. Overall, the cytotoxicity associated with NRH supplementation appears to be independent of ROS generation. Strikingly, NRH supplementation enhanced cytotoxicity of carboplatin in OVCAR8, but not ES2 or SKOV3. Paclitaxel cytotoxicity was also enhanced by the addition of NRH in OVCAR8, but not ES2 or SKOV3 cell lines. NA supplementation had no effect on baseline treatment-induced cytotoxicity. PARP inhibition by olaparib requires NAD+. Interestingly, NRH supplementation enhanced olaparib cytotoxicity in SKOV3 and OVCAR8, but not ES2 cells. NRH in combination with olaparib completely altered mitochondrial respiration, thereby shutting down energy consumption, which would lead to cell death. Coupled together with expression data of key enzymes required for NRH/NAD metabolism, this could be key in understanding mechanisms of cell death with NRH supplementation. Here, we showed that in the context of EOC, exploitation of the NAD+ bioenergetic phenotype through NRH supplementation is a biologically feasible strategy to enhance the response of traditional therapy with potentially minimal toxicity. These data suggest several potential mechanisms by which cellular NAD+ availability impacts treatment efficacy and resistance and highlights the potential utility of NAD+ metabolomics as a biomarker to guide treatment decisions. Full article
(This article belongs to the Special Issue New Aspects of Bioenergetics in Cancer)
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