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Biomedicines
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Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives
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Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives

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

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 17745

Special Issue Editor

Dr. Francesco Ciccarese

E-Mail Website
Guest Editor
Istituto Oncologico Veneto IOV-IRCCS, via Gattamelata 64, 35128 Padova, Italy
Interests: reactive oxygen species; redox homeostasis; electron transport chain; mitochondria; cancer metabolism; apoptosis; anticancer strategies; autophagy; drug development; viruses; angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic rewiring is a common feature of cancer cells, which promotes tumorigenesis by sustaining uncontrolled proliferation, survival in an adverse microenvironment, invasion, metastasis, and resistance to anticancer therapies. Cancer cells tightly control catabolic and anabolic reactions through a plethora of processes, including oncogenic activation, loss of tumor suppressors, genetic alterations in metabolic genes, epigenetic regulation, and modulation by both microRNAs and long non-coding RNAs. Moreover, there is evidence that oncogenic viruses also impinge on these pathways to induce malignant transformation. Evasion of cell death is the leading cause of therapeutic failure. In this regard, cancer metabolism impacts on the response of cancer cells to treatment by activating pro-survival processes, including autophagy, or favoring immune escape by modulating the tumor microenvironment. The pivotal role of metabolic reprogramming in the resistance of cancer cells to different types of cell death, including apoptosis and ferroptosis, provides the rationale for anticancer strategies aimed at rewiring cancer cell metabolism. Such approaches have the potential to enhance the sensitivity of cancer cells to conventional and targeted therapies. This Special Issue of Biomedicines aims at dissecting the multifaceted connections between cancer metabolism and cell death pathways, with a focus on the pharmacological modulation of tumor metabolism as an anticancer strategy.

Dr. Francesco Ciccarese
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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
  • cell death
  • oncogenic activation
  • miRNAs and lncRNAs
  • oncogenic viruses
  • sensitization to anticancer therapies

Related Special Issue

Published Papers (7 papers)

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Editorial

Jump to: Research, Review

3 pages, 183 KiB  
Editorial
Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives
by Francesco Ciccarese
Biomedicines 2022, 10(8), 1828; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10081828 - 29 Jul 2022
Cited by 2 | Viewed by 949
Abstract
Deregulation of metabolism and resistance to cell death are two hallmarks of cancer [...] Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives)

Research

Jump to: Editorial, Review

14 pages, 2736 KiB  
Article
Reduction of Rapid Proliferating Tumour Cell Lines by Inhibition of the Specific Glycine Transporter GLYT1
by Christine Garcia Bierhals, Alison Howard and Barry H. Hirst
Biomedicines 2021, 9(12), 1770; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9121770 - 25 Nov 2021
Cited by 2 | Viewed by 1444
Abstract
Studies have highlighted the relevance of extracellular glycine and serine in supporting high growth rates of rapidly proliferating tumours. The present study analysed the role of the specific glycine transporter GLYT1 in supplying glycine to cancer cells and maintaining cell proliferation. GLYT1 knockdown [...] Read more.
Studies have highlighted the relevance of extracellular glycine and serine in supporting high growth rates of rapidly proliferating tumours. The present study analysed the role of the specific glycine transporter GLYT1 in supplying glycine to cancer cells and maintaining cell proliferation. GLYT1 knockdown in the rapidly proliferating tumour cell lines A549 and HT29 reduced the number of viable cells by approximately 30% and the replication rate presented a decrease of about 50% when compared to cells transfected with control siRNA. In contrast, when compared to control, GLYT1 siRNA had only a minimal effect on cell number of the slowly proliferating tumour cell line A498, reducing the number of viable cells by 7% and no significant difference was observed when analysing the replication rate between GLYT1 knockdown and control group. When utilising a specific GLYT1 inhibitor, ALX-5407, the doubling time of rapidly proliferating cells increased by about 8 h presenting a significant reduction in the number of viable cells after 96 h treatment when compared to untreated cells. Therefore, these results suggest that GLYT1 is required to maintain high proliferation rates in rapidly proliferating cancer cells and encourage further investigation of GLYT1 as a possible target in a novel therapeutic approach. Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives)
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16 pages, 5043 KiB  
Article
808-nm Photobiomodulation Affects the Viability of a Head and Neck Squamous Carcinoma Cellular Model, Acting on Energy Metabolism and Oxidative Stress Production
by Silvia Ravera, Nadia Bertola, Claudio Pasquale, Silvia Bruno, Stefano Benedicenti, Sara Ferrando, Angelina Zekiy, Praveen Arany and Andrea Amaroli
Biomedicines 2021, 9(11), 1717; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9111717 - 18 Nov 2021
Cited by 17 | Viewed by 2320
Abstract
Photobiomodulation (PBM) is a form of low-dose light therapy that acts through energy delivery from non-ionizing sources. During the recent two decades, there has been tremendous progress with PBM acceptance in medicine. However, PBM effects on potential stimulation of existing malignant or pre-malignant [...] Read more.
Photobiomodulation (PBM) is a form of low-dose light therapy that acts through energy delivery from non-ionizing sources. During the recent two decades, there has been tremendous progress with PBM acceptance in medicine. However, PBM effects on potential stimulation of existing malignant or pre-malignant cells remain unknown. Thus, the primary endpoint was to assess the safety of PBM treatment parameters on head and neck squamous cell carcinoma (HNSCC) proliferation or survival. The secondary endpoint was to assess any putative anti-cancer effects of PBM treatments. Cell viability, energy metabolism, oxidative stress, and pro- and anti-apoptotic markers expression were investigated on a Human Head and Neck Squamous Cell Carcinoma cellular model (OHSU-974 FAcorr cell line). PBM therapy was administered through the 810 nm diode laser (GaAlAs) device (Garda Laser, 7024 Negrar, Verona, Italy) at the powers of 0, 0.25, 0.50, 0.75, 1.00, or 1.25 W in continuous wave (CW) mode for an exposure time of 60 s with a spot-size of 1 cm2 and with a distance of 1.86 cm from the cells. Results showed that 810-nm PBM affected oxidative phosphorylation in OHSU-971 FAcorr, causing a metabolic switch to anaerobic glycolysis. In addition, PBM reduced the catalase activity, determining an unbalance between oxidative stress production and the antioxidant defenses, which could stimulate the pro-apoptotic cellular pathways. Our data, at the parameters investigated, suggest the safeness of PBM as a supportive cancer therapy. Pre-clinical and clinical studies are necessary to confirm the in vitro evidence. Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives)
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Review

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17 pages, 862 KiB  
Review
2-Hydroxyglutarate in Acute Myeloid Leukemia: A Journey from Pathogenesis to Therapies
by Vittoria Raimondi, Giulia Ciotti, Michele Gottardi and Francesco Ciccarese
Biomedicines 2022, 10(6), 1359; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10061359 - 09 Jun 2022
Cited by 8 | Viewed by 2200
Abstract
The oncometabolite 2-hydroxyglutarate (2-HG) plays a key role in differentiation blockade and metabolic reprogramming of cancer cells. Approximatively 20–30% of acute myeloid leukemia (AML) cases carry mutations in the isocitrate dehydrogenase (IDH) enzymes, leading to a reduction in the Krebs cycle intermediate α-ketoglutarate [...] Read more.
The oncometabolite 2-hydroxyglutarate (2-HG) plays a key role in differentiation blockade and metabolic reprogramming of cancer cells. Approximatively 20–30% of acute myeloid leukemia (AML) cases carry mutations in the isocitrate dehydrogenase (IDH) enzymes, leading to a reduction in the Krebs cycle intermediate α-ketoglutarate (α-KG) to 2-HG. Relapse and chemoresistance of AML blasts following initial good response to standard therapy account for the very poor outcome of this pathology, which represents a great challenge for hematologists. The decrease of 2-HG levels through pharmacological inhibition of mutated IDH enzymes induces the differentiation of AML blasts and sensitizes leukemic cells to several anticancer drugs. In this review, we provide an overview of the main genetic mutations in AML, with a focus on IDH mutants and the role of 2-HG in AML pathogenesis. Moreover, we discuss the impact of high levels of 2-HG on the response of AML cells to antileukemic therapies and recent evidence for highly efficient combinations of mutant IDH inhibitors with other drugs for the management of relapsed/refractory (R/R) AML. Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives)
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34 pages, 2628 KiB  
Review
Targeting the Interplay between Cancer Metabolic Reprogramming and Cell Death Pathways as a Viable Therapeutic Path
by Elisabetta Iessi, Rosa Vona, Camilla Cittadini and Paola Matarrese
Biomedicines 2021, 9(12), 1942; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9121942 - 18 Dec 2021
Cited by 6 | Viewed by 3638
Abstract
In cancer cells, metabolic adaptations are often observed in terms of nutrient absorption, biosynthesis of macromolecules, and production of energy necessary to meet the needs of the tumor cell such as uncontrolled proliferation, dissemination, and acquisition of resistance to death processes induced by [...] Read more.
In cancer cells, metabolic adaptations are often observed in terms of nutrient absorption, biosynthesis of macromolecules, and production of energy necessary to meet the needs of the tumor cell such as uncontrolled proliferation, dissemination, and acquisition of resistance to death processes induced by both unfavorable environmental conditions and therapeutic drugs. Many oncogenes and tumor suppressor genes have a significant effect on cellular metabolism, as there is a close relationship between the pathways activated by these genes and the various metabolic options. The metabolic adaptations observed in cancer cells not only promote their proliferation and invasion, but also their survival by inducing intrinsic and acquired resistance to various anticancer agents and to various forms of cell death, such as apoptosis, necroptosis, autophagy, and ferroptosis. In this review we analyze the main metabolic differences between cancer and non-cancer cells and how these can affect the various cell death pathways, effectively determining the susceptibility of cancer cells to therapy-induced death. Targeting the metabolic peculiarities of cancer could represent in the near future an innovative therapeutic strategy for the treatment of those tumors whose metabolic characteristics are known. Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives)
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22 pages, 386 KiB  
Review
The Role of Metabolism in Tumor Immune Evasion: Novel Approaches to Improve Immunotherapy
by Alberto Cruz-Bermúdez, Raquel Laza-Briviesca, Marta Casarrubios, Belén Sierra-Rodero and Mariano Provencio
Biomedicines 2021, 9(4), 361; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9040361 - 31 Mar 2021
Cited by 7 | Viewed by 2731
Abstract
The tumor microenvironment exhibits altered metabolic properties as a consequence of the needs of tumor cells, the natural selection of the most adapted clones, and the selfish relationship with other cell types. Beyond its role in supporting uncontrolled tumor growth, through energy and [...] Read more.
The tumor microenvironment exhibits altered metabolic properties as a consequence of the needs of tumor cells, the natural selection of the most adapted clones, and the selfish relationship with other cell types. Beyond its role in supporting uncontrolled tumor growth, through energy and building materials obtention, metabolism is a key element controlling tumor immune evasion. Immunotherapy has revolutionized the treatment of cancer, being the first line of treatment for multiple types of malignancies. However, many patients either do not benefit from immunotherapy or eventually relapse. In this review we overview the immunoediting process with a focus on the metabolism-related elements that are responsible for increased immune evasion, either through reduced immunogenicity or increased resistance of tumor cells to the apoptotic action of immune cells. Finally, we describe the main molecules to modulate these immune evasion processes through the control of the metabolic microenvironment as well as their clinical developmental status. Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives)
13 pages, 816 KiB  
Review
Endogenous Anti-Cancer Candidates in GPCR, ER Stress, and EMT
by Rohit Gundamaraju, Wenying Lu, Iman Azimi, Rajaraman Eri and Sukhwinder Singh Sohal
Biomedicines 2020, 8(10), 402; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8100402 - 09 Oct 2020
Cited by 10 | Viewed by 3470
Abstract
The majority of cellular responses to external stimuli are mediated by receptors such as G protein-coupled receptors (GPCRs) and systems including endoplasmic reticulum stress (ER stress). Since GPCR signalling is pivotal in numerous malignancies, they are widely targeted by a number of clinical [...] Read more.
The majority of cellular responses to external stimuli are mediated by receptors such as G protein-coupled receptors (GPCRs) and systems including endoplasmic reticulum stress (ER stress). Since GPCR signalling is pivotal in numerous malignancies, they are widely targeted by a number of clinical drugs. Cancer cells often negatively modulate GPCRs in order to survive, proliferate and to disseminate. Similarly, numerous branches of the unfolded protein response (UPR) act as pro-survival mediators and are involved in promoting cancer progression via mechanisms such as epithelial to mesenchymal transition (EMT). However, there are a few proteins among these groups which impede deleterious effects by orchestrating the pro-apoptotic phenomenon and paving a therapeutic pathway. The present review exposes and discusses such critical mechanisms and some of the key processes involved in carcinogenesis. Full article
(This article belongs to the Special Issue Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives)
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