Energy Metabolism in Cancers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 5205

Special Issue Editor


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Guest Editor
Department of Internal Medicine, Ewha Womans University Medical Center, Ewha Womans University College of Medicine, Seoul 07804, Republic of Korea
Interests: anticancer therapy for hepatocellular carcinoma or other cancers; glycolysis; mitochondrial oxidation; energy metabolism; metastasis; epithelial to mesenchymal transition; chemo-resistance

Special Issue Information

Dear Colleagues,

Over the course of several decades, the survival of patients with cancers has increased due to advances in anticancer therapy such as immunotherapy (PD-1 blockade), tyrosine kinase inhibitors (sorafenib, lenvatinib, regorafenib, cabozantinib), or their combination therapy. However, the overall survival of cancer patients is still not satisfactory. Accordingly, we need a different point of view for anticancer therapy based on recent approaches in cancers. Energy metabolism is the process of generating energy in the form of adenosine triphosphate (ATP) from nutrients, including both glycolysis and mitochondrial respiration including fatty acid and amino acid metabolism. The metabolic pathways are highly regulated and interconnected to maintain ATP production in order to sustain all fundamental cellular processes in cancers. Cancer cells are known to exhibit dysregulated metabolic pathways, which contribute to metabolic flexibility that promotes aberrant cell proliferation and survival even under difficult conditions such as hypoxia. Given the critical importance of energy metabolism in cancers, alterations in key metabolic pathways lead to the development and progression of cancers. In contrast, energy depletion in cancers is one of the major triggers of the cancer cell death cascade and dysfunction of mitochondria. This Special Issue, entitled “Energy Metabolism in Cancers”, aims to present a collection of original research articles (basic, translational, or clinical) and reviews that address the molecular and cellular biology underlying various pathways in energy metabolism that contribute to the progression of cancers, or their initiation and metastasis. Studies on compounds that modulate energy metabolism as strategies to suppress cancer progression, metastasis, and resistance to anticancer therapy will also be considered.

Dr. Minjong Lee
Guest Editor

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Keywords

  • Warburg effect
  • mitochondrial oxidation
  • energy metabolism
  • metastasis
  • chemo-resistance
  • glutamine
  • fatty acid

Published Papers (2 papers)

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Research

26 pages, 4542 KiB  
Article
Unveiling Metabolic Vulnerability and Plasticity of Human Osteosarcoma Stem and Differentiated Cells to Improve Cancer Therapy
by Gerardo Della Sala, Consiglia Pacelli, Francesca Agriesti, Ilaria Laurenzana, Francesco Tucci, Mirko Tamma, Nazzareno Capitanio and Claudia Piccoli
Biomedicines 2022, 10(1), 28; https://doi.org/10.3390/biomedicines10010028 - 23 Dec 2021
Cited by 7 | Viewed by 2785
Abstract
Defining the metabolic phenotypes of cancer-initiating cells or cancer stem cells and of their differentiated counterparts might provide fundamental knowledge for improving or developing more effective therapies. In this context we extensively characterized the metabolic profiles of two osteosarcoma-derived cell lines, the 3AB-OS [...] Read more.
Defining the metabolic phenotypes of cancer-initiating cells or cancer stem cells and of their differentiated counterparts might provide fundamental knowledge for improving or developing more effective therapies. In this context we extensively characterized the metabolic profiles of two osteosarcoma-derived cell lines, the 3AB-OS cancer stem cells and the parental MG-63 cells. To this aim Seahorse methodology-based metabolic flux analysis under a variety of conditions complemented with real time monitoring of cell growth by impedentiometric technique and confocal imaging were carried out. The results attained by selective substrate deprivation or metabolic pathway inhibition clearly show reliance of 3AB-OS on glycolysis and of MG-63 on glutamine oxidation. Treatment of the osteosarcoma cell lines with cisplatin resulted in additive inhibitory effects in MG-63 cells depleted of glutamine whereas it antagonized under selective withdrawal of glucose in 3AB-OS cells thereby manifesting a paradoxical pro-survival, cell-cycle arrest in S phase and antioxidant outcome. All together the results of this study highlight that the efficacy of specific metabolite starvation combined with chemotherapeutic drugs depends on the cancer compartment and suggest cautions in using it as a generalizable curative strategy. Full article
(This article belongs to the Special Issue Energy Metabolism in Cancers)
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18 pages, 28968 KiB  
Article
Endothelial Heme Dynamics Drive Cancer Cell Metabolism by Shaping the Tumor Microenvironment
by Sara Petrillo, Francesco De Giorgio, Joanna Kopecka, Tullio Genova, Veronica Fiorito, Anna Lucia Allocco, Francesca Bertino, Deborah Chiabrando, Federico Mussano, Fiorella Altruda, Luca Munaron, Chiara Riganti and Emanuela Tolosano
Biomedicines 2021, 9(11), 1557; https://doi.org/10.3390/biomedicines9111557 - 28 Oct 2021
Cited by 6 | Viewed by 1919
Abstract
The crosstalk among cancer cells (CCs) and stromal cells within the tumor microenvironment (TME) has a prominent role in cancer progression. The significance of endothelial cells (ECs) in this scenario relies on multiple vascular functions. By forming new blood vessels, ECs support tumor [...] Read more.
The crosstalk among cancer cells (CCs) and stromal cells within the tumor microenvironment (TME) has a prominent role in cancer progression. The significance of endothelial cells (ECs) in this scenario relies on multiple vascular functions. By forming new blood vessels, ECs support tumor growth. In addition to their angiogenic properties, tumor-associated ECs (TECs) establish a unique vascular niche that actively modulates cancer development by shuttling a selected pattern of factors and metabolites to the CC. The profile of secreted metabolites is strictly dependent on the metabolic status of the cell, which is markedly perturbed in TECs. Recent evidence highlights the involvement of heme metabolism in the regulation of energy metabolism in TECs. The present study shows that interfering with endothelial heme metabolism by targeting the cell membrane heme exporter Feline Leukemia Virus subgroup C Receptor 1a (FLVCR1a) in TECs, resulted in enhanced fatty acid oxidation (FAO). Moreover, FAO-derived acetyl-CoA was partly consumed through ketogenesis, resulting in ketone bodies (KBs) accumulation in FLVCR1a-deficient TECs. Finally, the results from this study also demonstrate that TECs-derived KBs can be secreted in the extracellular environment, inducing a metabolic rewiring in the CC. Taken together, these data may contribute to finding new metabolic vulnerabilities for cancer therapy. Full article
(This article belongs to the Special Issue Energy Metabolism in Cancers)
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