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Cancers
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Metabolic Reprogramming for Cancer Immunotherapy
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Metabolic Reprogramming for Cancer Immunotherapy

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 23647

Special Issue Editors

Dr. Marion R. Curtis

E-Mail Website
Guest Editor
Department of Immunology, Mayo Clinic, Scottsdale, Arizona, USA
Interests: tumor microenvironment; cancer immunotherapy; metabolism; ovarian cancer; metastasis
Dr. Abhinav P. Acharya

E-Mail Website
Guest Editor
School for the Engineering of Matter, Transport and Energy Arizona State University, Tempe, AZ, USA
Interests: immunoengineering; biomaterials; innovating point-of-care diagnostics; drug delivery

Special Issue Information

Dear Colleagues,

Recent findings in the field of immunology have demonstrated that diverse immune cell types reprogram their metabolism to meet the demands of activation and differentiation. This metabolic reprogramming is similar to the phenotype demonstrated by cancer cells, which shift their metabolism from oxidative phosphorylation towards aerobic glycolysis to generate the metabolic intermediates required to meet the demands of proliferation, invasion, and survival within the tumor microenvironment.

Currently, we do not fully understand the consequences of the changes in metabolic pathways and substrates utilized by immune cells in the tumor microenvironment that would direct the development of rational metabolic interventions to enhance the effectiveness of immunotherapy.

We invite both primary research and review articles that (1) focus on a mechanistic understanding of the metabolic processes in immune cells that support anti-tumor responses, (2) determine how the tumor microenvironment affects immune effector functions through cell-to-cell interactions or changes in metabolic substrates, and (3) focus on novel methods to reprogram the metabolic pathways used by immune cells to improve cancer immunotherapy.

Dr. Marion R. Curtis
Dr. Abhinav P. Acharya
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 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

  • immunometabolism
  • bioengineering
  • metabolic reprogramming
  • adaptive immunity
  • innate immunity
  • adoptive cell therapy

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Published Papers (5 papers)

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Review

19 pages, 1481 KiB  
Review
Instruction of Immunometabolism by Adipose Tissue: Implications for Cancer Progression
by Remya Raja, Christopher Wu, Francesca Limbeck, Kristina Butler, Abhinav P. Acharya and Marion Curtis
Cancers 2021, 13(13), 3327; https://doi.org/10.3390/cancers13133327 - 2 Jul 2021
Cited by 4 | Viewed by 4101
Abstract
Disruption of metabolic homeostasis at the organismal level can cause metabolic syndrome associated with obesity. The role of adipose tissue in cancer has been investigated over the last several decades with many studies implicating obesity as a risk factor for the development of [...] Read more.
Disruption of metabolic homeostasis at the organismal level can cause metabolic syndrome associated with obesity. The role of adipose tissue in cancer has been investigated over the last several decades with many studies implicating obesity as a risk factor for the development of cancer. Adipose tissue contains a diverse array of immune cell populations that promote metabolic homeostasis through a tightly controlled balance of pro- and anti-inflammatory signals. During obesity, pro-inflammatory cell types infiltrate and expand within the adipose tissue, exacerbating metabolic dysfunction. Some studies have now shown that the intracellular metabolism of immune cells is also deregulated by the lipid-rich environment in obesity. What is not fully understood, is how this may influence cancer progression, metastasis, and anti-tumor immunity. This review seeks to highlight our current understanding of the effect of adipose tissue on immune cell function and discuss how recent results offer new insight into the role that adipose tissue plays in cancer progression and anti-tumor immunity. Full article
(This article belongs to the Special Issue Metabolic Reprogramming for Cancer Immunotherapy)
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25 pages, 823 KiB  
Review
Metabolic Reprogramming by Reduced Calorie Intake or Pharmacological Caloric Restriction Mimetics for Improved Cancer Immunotherapy
by Erwan Eriau, Juliette Paillet, Guido Kroemer and Jonathan G. Pol
Cancers 2021, 13(6), 1260; https://doi.org/10.3390/cancers13061260 - 12 Mar 2021
Cited by 16 | Viewed by 5661
Abstract
Caloric restriction and fasting have been known for a long time for their health- and life-span promoting effects, with coherent observations in multiple model organisms as well as epidemiological and clinical studies. This holds particularly true for cancer. The health-promoting effects of caloric [...] Read more.
Caloric restriction and fasting have been known for a long time for their health- and life-span promoting effects, with coherent observations in multiple model organisms as well as epidemiological and clinical studies. This holds particularly true for cancer. The health-promoting effects of caloric restriction and fasting are mediated at least partly through their cellular effects—chiefly autophagy induction—rather than reduced calorie intake per se. Interestingly, caloric restriction has a differential impact on cancer and healthy cells, due to the atypical metabolic profile of malignant tumors. Caloric restriction mimetics are non-toxic compounds able to mimic the biochemical and physiological effects of caloric restriction including autophagy induction. Caloric restriction and its mimetics induce autophagy to improve the efficacy of some cancer treatments that induce immunogenic cell death (ICD), a type of cellular demise that eventually elicits adaptive antitumor immunity. Caloric restriction and its mimetics also enhance the therapeutic efficacy of chemo-immunotherapies combining ICD-inducing agents with immune checkpoint inhibitors targeting PD-1. Collectively, preclinical data encourage the application of caloric restriction and its mimetics as an adjuvant to immunotherapies. This recommendation is subject to confirmation in additional experimental settings and in clinical trials. In this work, we review the preclinical and clinical evidence in favor of such therapeutic interventions before listing ongoing clinical trials that will shed some light on this subject. Full article
(This article belongs to the Special Issue Metabolic Reprogramming for Cancer Immunotherapy)
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14 pages, 1096 KiB  
Review
Role of Bladder Cancer Metabolic Reprogramming in the Effectiveness of Immunotherapy
by Mathijs P. Scholtes, Florus C. de Jong, Tahlita C. M. Zuiverloon and Dan Theodorescu
Cancers 2021, 13(2), 288; https://doi.org/10.3390/cancers13020288 - 14 Jan 2021
Cited by 12 | Viewed by 3363
Abstract
Metabolic reprogramming (MR) is an upregulation of biosynthetic and bioenergetic pathways to satisfy increased energy and metabolic building block demands of tumors. This includes glycolytic activity, which deprives the tumor microenvironment (TME) of nutrients while increasing extracellular lactic acid. This inhibits cytotoxic immune [...] Read more.
Metabolic reprogramming (MR) is an upregulation of biosynthetic and bioenergetic pathways to satisfy increased energy and metabolic building block demands of tumors. This includes glycolytic activity, which deprives the tumor microenvironment (TME) of nutrients while increasing extracellular lactic acid. This inhibits cytotoxic immune activity either via direct metabolic competition between cancer cells and cytotoxic host cells or by the production of immune-suppressive metabolites such as lactate or kynurenine. Since immunotherapy is a major treatment option in patients with metastatic urothelial carcinoma (UC), MR may have profound implications for the success of such therapy. Here, we review how MR impacts host immune response to UC and the impact on immunotherapy response (including checkpoint inhibitors, adaptive T cell therapy, T cell activation, antigen presentation, and changes in the tumor microenvironment). Articles were identified by literature searches on the keywords or references to “UC” and “MR”. We found several promising therapeutic approaches emerging from preclinical models that can circumvent suppressive MR effects on the immune system. A select summary of active clinical trials is provided with examples of possible options to enhance the effectiveness of immunotherapy. In conclusion, the literature suggests manipulating the MR is feasible and may improve immunotherapy effectiveness in UC. Full article
(This article belongs to the Special Issue Metabolic Reprogramming for Cancer Immunotherapy)
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17 pages, 1577 KiB  
Review
Manipulation of Glucose Availability to Boost Cancer Immunotherapies
by Federica Marchesi, Debora Vignali, Beatrice Manini, Alessandra Rigamonti and Paolo Monti
Cancers 2020, 12(10), 2940; https://doi.org/10.3390/cancers12102940 - 12 Oct 2020
Cited by 16 | Viewed by 2919
Abstract
The orchestration of T cell responses is intimately linked to the execution of metabolic processes, both in homeostasis and disease. In cancer tissues, metabolic alterations that characterize malignant transformation profoundly affect the composition of the immune microenvironment and the accomplishment of an effective [...] Read more.
The orchestration of T cell responses is intimately linked to the execution of metabolic processes, both in homeostasis and disease. In cancer tissues, metabolic alterations that characterize malignant transformation profoundly affect the composition of the immune microenvironment and the accomplishment of an effective anti-tumor response. The growing understanding of the metabolic regulation of immune cell function has shed light on the possibility to manipulate metabolic pathways as a strategy to improve T cell function in cancer. Among others, glucose metabolism through the glycolytic pathway is central in shaping T cell responses and emerges as an ideal target to improve cancer immunotherapy. However, metabolic manipulation requires a deep level of control over side-effects and development of biomarkers of response. Here, we summarize the metabolic control of T cell function and focus on the implications of metabolic manipulation for the design of immunotherapeutic strategies. Integrating our understanding of T cell function and metabolism will hopefully foster the forthcoming development of more effective immunotherapeutic strategies. Full article
(This article belongs to the Special Issue Metabolic Reprogramming for Cancer Immunotherapy)
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12 pages, 2302 KiB  
Review
MR1-Restricted T Cells in Cancer Immunotherapy
by Pedro Flores-Villanueva, Navid Sobhani, Xu Wang and Yong Li
Cancers 2020, 12(8), 2145; https://doi.org/10.3390/cancers12082145 - 3 Aug 2020
Cited by 8 | Viewed by 6710
Abstract
Major histocompatibility complex class I-related (MR1) was first identified as a cell membrane protein involved in the development and expansion of a unique set of T cells expressing an invariant T-cell receptor (TCR) α-chain. These cells were initially discovered in mucosal tissues, such [...] Read more.
Major histocompatibility complex class I-related (MR1) was first identified as a cell membrane protein involved in the development and expansion of a unique set of T cells expressing an invariant T-cell receptor (TCR) α-chain. These cells were initially discovered in mucosal tissues, such as the intestinal mucosa, so they are called mucosal-associated invariant T (MAIT) cells. MR1 senses the presence of intermediate metabolites of riboflavin and folic acid synthesis that have been chemically modified by the side-products of glycolysis, glyoxal or methylglyoxal. These modified metabolites form complexes with MR1 and translocate from the endoplasmic reticulum to the plasma membrane where MAIT cells’ TCRs recognize them. Recent publications report that atypical MR1-restricted cytotoxic T cells, differing from MAIT cells in TCR usage, antigen, and transcription factor profile, recognize an as yet unknown cancer-specific metabolite presented by MR1 in cancer cells. This metabolite may represent another class of neoantigens, beyond the neo-peptides arising from altered tumor proteins. In an MR1-dependent manner, these MR1-restricted T cells, while sparing noncancerous cells, kill many cancer cell lines and attenuate cell-line-derived and patient-derived xenograft tumors. As MR1 is monomorphic and expressed in a wide range of cancer tissues, these findings raise the possibility of universal pan-cancer immunotherapies that are dependent on cancer metabolites. Full article
(This article belongs to the Special Issue Metabolic Reprogramming for Cancer Immunotherapy)
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