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Cancers
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Novel Metabolic Approaches Targeting Cancer Cells
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Novel Metabolic Approaches Targeting Cancer Cells

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 16369

Special Issue Editors

Dr. Bela Ozsvari

E-Mail Website
Guest Editor
Translational Medicine, School of Science, Engineering and Environment (SEE), University of Salford, Manchester, UK
Interests: breast cancer; mitochondria; cancer stem cells; senescence; drug screening
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Michael Lisanti

E-Mail Website
Guest Editor
Translational Medicine, School of Science, Engineering and the Environment (SEE), University of Salford, Greater Manchester, M5 4WT, UK
Interests: cancer stem cells; cancer metabolism; tumour recurrence and metastasis; drug resistance; clinical trials
Dr. Anna Sebestyèn

E-Mail Website
Guest Editor
I. Institute of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary
Interests: Signaling Pathways; Xenograft Model; In Vitro Culture; TGF-beta; mTOR; Cells; Apoptosis; Caspase; Tumor Metabolism

Special Issue Information

Dear Colleagues,

Metabolic reprogramming is one of the main hallmarks of cancer. Numerous studies have shown that the metabolic phenotype of cells within tumors is heterogeneous and distinct from their normal counterparts. Furthermore, altered metabolism has been recognized as one of the major mechanisms of resistance to current therapies. Thus, targeting the metabolic differences between tumor and normal cells holds promise as a novel anticancer strategy.

The purpose of this Special Issue is to discuss the latest research of the metabolic reprogramming of cancer cells, particularly focusing on metabolic vulnerabilities that might be future therapeutical targets. This Special Issue welcomes original research articles, as well as reviews.

Dr. Bela Ozsvari
Prof. Dr. Michael Lisanti
Dr. Anna Sebestyèn
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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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

  • cancer metabolism
  • metastasis
  • tumor heterogeneity
  • cancer stem cells
  • drug resistance

Published Papers (6 papers)

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Editorial

Jump to: Research, Review

3 pages, 205 KiB  
Editorial
Novel Metabolic Approaches Targeting Cancer Cells
by Anna Sebestyén, Michael P. Lisanti and Bela Ozsvari
Cancers 2023, 15(22), 5448; https://doi.org/10.3390/cancers15225448 - 16 Nov 2023
Viewed by 741
Abstract
Metabolic reprogramming is one of the main hallmarks of cancer [...] Full article
(This article belongs to the Special Issue Novel Metabolic Approaches Targeting Cancer Cells)

Research

Jump to: Editorial, Review

19 pages, 3076 KiB  
Article
Extracellular Vesicle-Mediated Metastasis Suppressors NME1 and NME2 Modify Lipid Metabolism in Fibroblasts
by Barbara Mátyási, Gábor Petővári, Titanilla Dankó, Henriett Butz, István Likó, Péter Lőw, Isabelle Petit, Randa Bittar, Dominique Bonnefont-Rousselot, Zsolt Farkas, Tamás Szeniczey, Kinga Molnár, Krisztina Pálóczi, Edit I. Buzás, Mathieu Boissan, Anna Sebestyén and Krisztina Takács-Vellai
Cancers 2022, 14(16), 3913; https://doi.org/10.3390/cancers14163913 - 13 Aug 2022
Cited by 2 | Viewed by 2251
Abstract
Nowadays, extracellular vesicles (EVs) raise a great interest as they are implicated in intercellular communication between cancer and stromal cells. Our aim was to understand how vesicular NME1 and NME2 released by breast cancer cells influence the tumour microenvironment. As a model, we [...] Read more.
Nowadays, extracellular vesicles (EVs) raise a great interest as they are implicated in intercellular communication between cancer and stromal cells. Our aim was to understand how vesicular NME1 and NME2 released by breast cancer cells influence the tumour microenvironment. As a model, we used human invasive breast carcinoma cells overexpressing NME1 or NME2, and first analysed in detail the presence of both isoforms in EV subtypes by capillary Western immunoassay (WES) and immunoelectron microscopy. Data obtained by both methods showed that NME1 was present in medium-sized EVs or microvesicles, whereas NME2 was abundant in both microvesicles and small-sized EVs or exosomes. Next, human skin-derived fibroblasts were treated with NME1 or NME2 containing EVs, and subsequently mRNA expression changes in fibroblasts were examined. RNAseq results showed that the expression of fatty acid and cholesterol metabolism-related genes was decreased significantly in response to NME1 or NME2 containing EV treatment. We found that FASN (fatty acid synthase) and ACSS2 (acyl-coenzyme A synthetase short-chain family member 2), related to fatty acid synthesis and oxidation, were underexpressed in NME1/2-EV-treated fibroblasts. Our data show an emerging link between NME-containing EVs and regulation of tumour metabolism. Full article
(This article belongs to the Special Issue Novel Metabolic Approaches Targeting Cancer Cells)
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12 pages, 1933 KiB  
Article
Extracellular Citrate Treatment Induces HIF1α Degradation and Inhibits the Growth of Low-Glycolytic Hepatocellular Carcinoma under Hypoxia
by Seon Yoo Kim, Dongwoo Kim, Jisu Kim, Hae Young Ko, Won Jin Kim, Youngjoo Park, Hye Won Lee, Dai Hoon Han, Kyung Sik Kim, Sunghyouk Park, Misu Lee and Mijin Yun
Cancers 2022, 14(14), 3355; https://doi.org/10.3390/cancers14143355 - 10 Jul 2022
Cited by 3 | Viewed by 2194
Abstract
HCC is well known for low glycolysis in the tumors, whereas hypoxia induces glycolytic phenotype and tumor progression. This study was conducted to evaluate the expression of SLCs in human HCCs and investigated whether extracellular nutrient administration related to SLCs in low-glycolytic HCC [...] Read more.
HCC is well known for low glycolysis in the tumors, whereas hypoxia induces glycolytic phenotype and tumor progression. This study was conducted to evaluate the expression of SLCs in human HCCs and investigated whether extracellular nutrient administration related to SLCs in low-glycolytic HCC can prevent hypoxic tumor progression. SLCs expression was screened according to the level of glycolysis in HCCs. Then, whether extracellular nutrient treatment can affect hypoxic tumor progression, as well as the mechanisms, were evaluated in an in vitro cell line and an in vivo animal model. Low-glycolytic HCCs showed high SLC13A5/NaCT and SLC16A1/MCT1 but low SLC2A1/GLUT1 and HIF1α/HIF1α expression. Especially, high SLC13A5 expression was significantly associated with good overall survival in the Cancer Genome Atlas (TCGA) database. In HepG2 cells with the highest NaCT expression, extracellular citrate treatment upon hypoxia induced HIF1α degradation, which led to reduced glycolysis and cellular proliferation. Finally, in HepG2-animal models, the citrate-treated group showed smaller tumor with less hypoxic areas than the vehicle-treated group. In patients with HCC, SLC13A5/NaCT is an important SLC, which is associated with low glycolysis and good prognosis. Extracellular citrate treatment induced the failure of metabolic adaptation to hypoxia and tumor growth inhibition, which can be a potential therapeutic strategy in HCCs. Full article
(This article belongs to the Special Issue Novel Metabolic Approaches Targeting Cancer Cells)
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19 pages, 3741 KiB  
Article
β-Hydroxy-β-Methylbutyrate Supplementation Promotes Antitumor Immunity in an Obesity Responsive Mouse Model of Pancreatic Ductal Adenocarcinoma
by Michael F. Coleman, Kristyn A. Liu, Alexander J. Pfeil, Suhas K. Etigunta, Xiaohu Tang, Salvador Fabela, Laura M. Lashinger, Zhengrong Cui and Stephen D. Hursting
Cancers 2021, 13(24), 6359; https://doi.org/10.3390/cancers13246359 - 18 Dec 2021
Cited by 1 | Viewed by 3658
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related deaths in the United States, and effective therapies for PDAC are currently lacking. Moreover, PDAC is promoted and exacerbated by obesity, while cachexia and sarcopenia are exceptionally common comorbidities that predict both [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related deaths in the United States, and effective therapies for PDAC are currently lacking. Moreover, PDAC is promoted and exacerbated by obesity, while cachexia and sarcopenia are exceptionally common comorbidities that predict both poor survival and treatment response. Managing PDAC with immunotherapies has thus far proven ineffective, partly due to the metabolically hostile tumor microenvironment. β-hydroxy-β-methylbutyrate (HMB), a metabolite of leucine commonly used as a dietary supplement to boost muscle growth and immune function, may be an attractive candidate to augment PDAC therapy. We therefore sought to test the hypothesis that HMB would enhance antitumor immunity while protecting mouse muscle mass. Control and diet-induced obese C57BL/6 male mice bearing subcutaneously injected Panc02 tumors were supplemented with 1% HMB and treated with or without 50 mg/kg gemcitabine (n = 15/group). HMB was associated with reduced muscle inflammation and increased muscle fiber size. HMB also reduced tumor growth and promoted antitumor immunity in obese, but not lean, mice, independent of the gemcitabine treatment. Separately, in lean tumor-bearing mice, HMB supplementation promoted an anti-PD1 immunotherapy response (n = 15/group). Digital cytometry implicated the decreased abundance of M2-like macrophages in PDAC tumors, an effect that was enhanced by anti-PD1 immunotherapy. We confirmed that HMB augments M1-like macrophage (antitumor) polarization. These preclinical findings suggest that HMB has muscle-sparing and antitumor activities against PDAC in the context of obesity, and that it may sensitize otherwise nonresponsive PDAC to immunotherapy. Full article
(This article belongs to the Special Issue Novel Metabolic Approaches Targeting Cancer Cells)
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Review

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26 pages, 1198 KiB  
Review
Succinate-Directed Approaches for Warburg Effect-Targeted Cancer Management, an Alternative to Current Treatments?
by Adrian Casas-Benito, Sonia Martínez-Herrero and Alfredo Martínez
Cancers 2023, 15(10), 2862; https://doi.org/10.3390/cancers15102862 - 22 May 2023
Cited by 4 | Viewed by 2472
Abstract
Approximately a century ago, Otto Warburg discovered that cancer cells use a fermentative rather than oxidative metabolism even though the former is more inefficient in terms of energy production per molecule of glucose. Cancer cells increase the use of this fermentative metabolism even [...] Read more.
Approximately a century ago, Otto Warburg discovered that cancer cells use a fermentative rather than oxidative metabolism even though the former is more inefficient in terms of energy production per molecule of glucose. Cancer cells increase the use of this fermentative metabolism even in the presence of oxygen, and this process is called aerobic glycolysis or the Warburg effect. This alternative metabolism is mainly characterized by higher glycolytic rates, which allow cancer cells to obtain higher amounts of total ATP, and the production of lactate, but there are also an activation of protumoral signaling pathways and the generation of molecules that favor cancer progression. One of these molecules is succinate, a Krebs cycle intermediate whose concentration is increased in cancer and which is considered an oncometabolite. Several protumoral actions have been associated to succinate and its role in several cancer types has been already described. Despite playing a major role in metabolism and cancer, so far, the potential of succinate as a target in cancer prevention and treatment has remained mostly unexplored, as most previous Warburg-directed anticancer strategies have focused on other intermediates. In this review, we aim to summarize succinate’s protumoral functions and discuss the use of succinate expression regulators as a potential cancer therapy strategy. Full article
(This article belongs to the Special Issue Novel Metabolic Approaches Targeting Cancer Cells)
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29 pages, 2188 KiB  
Review
Extracellular Vesicle-Mediated Mitochondrial Reprogramming in Cancer
by Roger Carles-Fontana, Nigel Heaton, Elena Palma and Shirin E. Khorsandi
Cancers 2022, 14(8), 1865; https://doi.org/10.3390/cancers14081865 - 7 Apr 2022
Cited by 7 | Viewed by 3674
Abstract
Altered metabolism is a defining hallmark of cancer. Metabolic adaptations are often linked to a reprogramming of the mitochondria due to the importance of these organelles in energy production and biosynthesis. Cancer cells present heterogeneous metabolic phenotypes that can be modulated by signals [...] Read more.
Altered metabolism is a defining hallmark of cancer. Metabolic adaptations are often linked to a reprogramming of the mitochondria due to the importance of these organelles in energy production and biosynthesis. Cancer cells present heterogeneous metabolic phenotypes that can be modulated by signals originating from the tumor microenvironment. Extracellular vesicles (EVs) are recognized as key players in intercellular communications and mediate many of the hallmarks of cancer via the delivery of their diverse biological cargo molecules. Firstly, this review introduces the most characteristic changes that the EV-biogenesis machinery and mitochondria undergo in the context of cancer. Then, it focuses on the EV-driven processes which alter mitochondrial structure, composition, and function to provide a survival advantage to cancer cells in the context of the hallmarks of cancers, such as altered metabolic strategies, migration and invasiveness, immune surveillance escape, and evasion of apoptosis. Finally, it explores the as yet untapped potential of targeting mitochondria using EVs as delivery vectors as a promising cancer therapeutic strategy. Full article
(This article belongs to the Special Issue Novel Metabolic Approaches Targeting Cancer Cells)
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