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Energy Metabolisms in Cancer
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Energy Metabolisms 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: closed (30 December 2023) | Viewed by 3036

Special Issue Editors

Prof. Dr. Giancarlo Solaini

E-Mail Website
Guest Editor
Department of Biomedical and Neuromotor Sciences, Alma Mater Studiorum University of Bologna, 40126 Bologna, Italy
Interests: cancer; bioenergetics; mitochondria; hypoxia; ischemia/reperfusion; ATP synthase; inhibitor protein IF1; ROS; antioxidant molecules
Special Issues, Collections and Topics in MDPI journals
Dr. Claudia Zanna

E-Mail Website
Guest Editor
Department of Biomedical Science and Neuromotor Sciences DIBINEM, University of Bologna | UNIBO, 40126 Bologna, Italy
Interests: cancer; OXPHOS; cellular biochemistry; mitochondrial disorders; mitochondria dynamics

Special Issue Information

Dear Colleagues,

The aim of this Special Issue on Energy Metabolisms in Cancer is to provide a short means of drawing attention to an immense topic, since each individual tumor and different cells within the same tumor may have different mechanisms of energy production and control.

Nonetheless, the investigation of bioenergetic pathways, or even of single reactions in a particular cell line, as well as the disclosure of the network interactions among the molecules that are involved may help to shed light on such complex systems. Notably, in recent years, energy metabolism has been considered as an additional hallmark of the cancer phenotype, and increasing knowledge of the molecular mechanisms responsible for metabolic shift in cancer cells may also be useful in understanding the onset of chemo- and radio-resistance.

In the complex and heterogeneous tumor ecosystem, cancer cells must acquire a flexible and variable metabolism to face and survive the many stress conditions, such as hypoxia, low glucose and other nutrient deficiencies, and exposure to low pH and high ROS levels. Therefore, tumor cells must reprogram their metabolism at many levels, and mitochondria play a pivotal role in this task, thus becoming essential to driving disease progression. It is generally accepted that many cancer cells change their metabolism, increasing cytosolic glycolysis, even in the presence of normal oxygen availability (the so-called Warburg effect), but more recent studies propose that this may occur in cells at certain stages, and it has also been clearly demonstrated that mitochondrial and oxidative metabolisms are relevant to growth and metastasis. Therefore, investigations of whether bioenergetic pathways are associated with mitochondria in cancer cells and whether their modulation is promoted by stressful conditions and/or microenvironment changes will be welcome in this Special Issue. Any studies that report endogenous molecules (proteins, metabolites, miRs, etc.) and exogenous molecules (drugs, plants metabolites, etc.) that are capable of interfering with pathways or single reactions in tumor cells and could help to unveil tumor biology and/or chemo- or radio-therapy are welcome.

We are pleased to invite you to submit research papers, reviews, communications, etc., for this Special Issue, “Energy Metabolisms in Cancer”, of International Journal of Molecular Sciences. We encourage authors to submit their experimental and theoretical results in as much detail as possible, including studies showing meaningful but negative results. We invite high-quality articles on basic and translational studies on tumor cells to be submitted before September 30, 2023.

Prof. Dr. Giancarlo Solaini
Dr. Claudia Zanna
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. 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

  • mitochondrial morphology and dynamics
  • oxidative phosphorylation complexes
  • reactive oxygen/nitrogen species
  • redox homeostasis
  • glucose metabolism
  • aminoacid metabolism
  • pyruvate/lactate metabolism
  • hypoxia/anoxia
  • anti-cancer drugs

Published Papers (2 papers)

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Research

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23 pages, 14087 KiB  
Article
The Pro-Oncogenic Protein IF1 Promotes Proliferation of Anoxic Cancer Cells during Re-Oxygenation
by Riccardo Righetti, Silvia Grillini, Valentina Del Dotto, Anna Costanzini, Francesca Liuzzi, Claudia Zanna, Gianluca Sgarbi, Giancarlo Solaini and Alessandra Baracca
Int. J. Mol. Sci. 2023, 24(19), 14624; https://doi.org/10.3390/ijms241914624 - 27 Sep 2023
Cited by 1 | Viewed by 897
Abstract
Cancer cells overexpress IF1, the endogenous protein that inhibits the hydrolytic activity of ATP synthase when mitochondrial membrane potential (ΔμH+) falls, as in ischemia. Other roles have been ascribed to IF1, but the associated molecular mechanisms [...] Read more.
Cancer cells overexpress IF1, the endogenous protein that inhibits the hydrolytic activity of ATP synthase when mitochondrial membrane potential (ΔμH+) falls, as in ischemia. Other roles have been ascribed to IF1, but the associated molecular mechanisms are still under debate. We investigated the ability of IF1 to promote survival and proliferation in osteosarcoma and colon carcinoma cells exposed to conditions mimicking ischemia and reperfusion, as occurs in vivo, particularly in solid tumors. IF1-silenced and parental cells were exposed to the FCCP uncoupler to collapse ΔμH+ and the bioenergetics of cell models were validated. All the uncoupled cells preserved mitochondrial mass, but the implemented mechanisms differed in IF1-expressing and IF1-silenced cells. Indeed, the membrane potential collapse and the energy charge preservation allowed an increase in both mitophagy and mitochondrial biogenesis in IF1-expressing cells only. Interestingly, the presence of IF1 also conferred a proliferative advantage to cells highly dependent on oxidative phosphorylation when the uncoupler was washed out, mimicking cell re-oxygenation. Overall, our results indicate that IF1, by allowing energy preservation and promoting mitochondrial renewal, can favor proliferation of anoxic cells and tumor growth. Therefore, hindering the action of IF1 may be promising for the therapy of tumors that rely on oxidative phosphorylation for energy production. Full article
(This article belongs to the Special Issue Energy Metabolisms in Cancer)
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Review

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16 pages, 1265 KiB  
Review
The Warburg Effect Explained: Integration of Enhanced Glycolysis with Heterogeneous Mitochondria to Promote Cancer Cell Proliferation
by Lilia Alberghina
Int. J. Mol. Sci. 2023, 24(21), 15787; https://doi.org/10.3390/ijms242115787 - 31 Oct 2023
Cited by 1 | Viewed by 1739
Abstract
The Warburg effect is the long-standing riddle of cancer biology. How does aerobic glycolysis, inefficient in producing ATP, confer a growth advantage to cancer cells? A new evaluation of a large set of literature findings covering the Warburg effect and its yeast counterpart, [...] Read more.
The Warburg effect is the long-standing riddle of cancer biology. How does aerobic glycolysis, inefficient in producing ATP, confer a growth advantage to cancer cells? A new evaluation of a large set of literature findings covering the Warburg effect and its yeast counterpart, the Crabtree effect, led to an innovative working hypothesis presented here. It holds that enhanced glycolysis partially inactivates oxidative phosphorylation to induce functional rewiring of a set of TCA cycle enzymes to generate new non-canonical metabolic pathways that sustain faster growth rates. The hypothesis has been structured by constructing two metabolic maps, one for cancer metabolism and the other for the yeast Crabtree effect. New lines of investigation, suggested by these maps, are discussed as instrumental in leading toward a better understanding of cancer biology in order to allow the development of more efficient metabolism-targeted anticancer drugs. Full article
(This article belongs to the Special Issue Energy Metabolisms in Cancer)
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