Mitochondria and Immunometabolism in Cancer

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

Deadline for manuscript submissions: 31 March 2025 | Viewed by 744

Special Issue Editors


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Guest Editor
Department of Sciences, University of Basilicata, Potenza, Italy
Interests: cell metabolism and mitochondrial metabolism; mitochondrial bioenergetics; redox alteration; enzymatic activity; inflammatory response and immunometabolism
Special Issues, Collections and Topics in MDPI journals

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Co-Guest Editor
Department of Science, University of Basilicata, Potenza, Italy
Interests: gene expression; transcriptional regulation; macrophage activation; immunometabolism
Special Issues, Collections and Topics in MDPI journals

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Co-Guest Editor
Department of Science, University of Basilicata, Potenza, Italy
Interests: transcriptional regulation; post-transcriptional regulation; miRNA; splicing mechanisms; liver
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, titled “Mitochondria and Immunometabolism in Cancer”, will focus on the role of mitochondria and their metabolic function in the crosstalk between cancer and immune cells.

A new perspective on the survival of cancer cells and the mechanisms underlying tumor progression has recently involved tumor microenvironmental cells. The hallmark of both cancer and activated immune cells is metabolic reprogramming, which depends on gene expression regulation in response to the rise in energetic demands and the need for specific metabolites. A focal point of these metabolic changes is the mitochondrial metabolism supplying energy and metabolites necessary for cell growth.

In this context, it is crucial to comprehend the relationship between cancer and microenvironmental cells, providing a new possible strategy for immunotreatments of cancer. We invite researchers to contribute to this Special Issue with original research or review articles focusing on mitochondrial metabolism, bioenergetics, mitochondrial signaling and immunometabolism in cancer.

This Special Issue includes, but is not limited to, the following topics:

  1. Immunometabolism;
  2. Bioenergetics;
  3. Mitochondrial metabolism;
  4. Cell signaling;
  5. Mitochondrial signaling;
  6. Cancer cell metabolism;
  7. Cancer cells- immune cells crosstalk;
  8. Gene expression regulation;
  9. Tumor microenvironment.

Dr. Simona Todisco
Dr. Santarsiero Anna
Dr. Paolo Convertini
Guest Editors

Manuscript Submission Information

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Keywords

  • immunometabolism
  • bioenergetics
  • mitochondrial metabolism
  • cell signaling
  • mitochondrial signaling
  • cancer cell metabolism
  • cancer cells–immune cells crosstalk
  • gene expression regulation
  • tumor microenvironment

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Published Papers (1 paper)

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Review

20 pages, 1363 KiB  
Review
Metabolic Crossroad Between Macrophages and Cancer Cells: Overview of Hepatocellular Carcinoma
by Anna Santarsiero, Paolo Convertini, Dominga Iacobazzi, Vittoria Infantino and Simona Todisco
Biomedicines 2024, 12(12), 2684; https://doi.org/10.3390/biomedicines12122684 - 25 Nov 2024
Viewed by 426
Abstract
The metabolic interplay between macrophages and cancer cells mirrors the plasticity of both kinds of cells, which adapt to the microenvironment by sustaining cell growth and proliferation. In this way, cancer cells induce macrophage polarization, and, on the other hand, tumor-associated macrophages (TAMs) [...] Read more.
The metabolic interplay between macrophages and cancer cells mirrors the plasticity of both kinds of cells, which adapt to the microenvironment by sustaining cell growth and proliferation. In this way, cancer cells induce macrophage polarization, and, on the other hand, tumor-associated macrophages (TAMs) contribute to the survival of cancer cells. In a simplified manner, macrophages can assume two opposite subtypes: M1, pro-inflammatory and anti-tumor phenotype, and M2, anti-inflammatory and protumor phenotype. How do cancer cells induce macrophage polarization? Any actor involved in tumor growth, including the mitochondria, releases molecules into the tumor microenvironment (TME) that trigger a subtype transition. These metabolic changes are the primary cause of this polarization. Hepatocellular carcinoma (HCC), the prevalent type of liver primary tumor, is characterized by cells with extensive metabolic adaptions due to high flexibility in different environmental conditions. This review focuses on the main metabolic features of M1 and M2 macrophages and HCC cells underlying their metabolic behavior in response to TME. Full article
(This article belongs to the Special Issue Mitochondria and Immunometabolism in Cancer)
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