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Cancers
Special Issues
Advances in Acidosis within the Tumor Microenvironment
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Advances in Acidosis within the Tumor Microenvironment

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 518

Special Issue Editors

Dr. Silvia Peppicelli

E-Mail Website
Guest Editor
Department of Experimental and Clinical Biomedical Sciences “Mario Serio”, University of Florence, 50134 Florence, Italy
Interests: tumor microenvironment; melanoma progression; cancer stem cells; tumor acidosis; tumor metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Elena Andreucci

E-Mail Website
Guest Editor
Department of Clinical and Experimental Biomedical Sciences “Mario Serio”, Section of Experimental Pathology and Oncology, University of Florence, V. le Morgagni, 50, 50134 Florence, Italy
Interests: tumor microenvironment; extracellular acidosis; tumor angiogenesis; tumor-derived extracellular vescicles (exososmes-ectososmes); cancer metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The discoveries of the last decade in the field of cancer research have shed light on the important role exerted by the local microenvironment that is established around the tumor mass in reprogramming the tumor cells toward aggressive phenotypes, contributing to disease advancement and metastasis. The term “tumor microenvironment” (TME) is very inclusive; when we discuss the TME, we refer not only to all the cellular and non-cellular stromal components within and surrounding the tumor mass, but also biochemical features such as hypoxia and acidosis that characterize most solid tumors. While hypoxia has been studied and characterized extensively, extracellular acidosis has drawn attention of the scientific community relatively recently, and much is yet to be defined. To date, strong evidence indicates that extracellular acidosis reprograms both cancer and stromal cells toward tumor progression by altering metabolism, therapy response, perfusion, immune surveillance and other key aspects, overall favoring the final metastatic dissemination. The aim of this Special Issue is to collect the most recent discoveries on acidic TME, with mechanistic insights and potential clinical interest.

For this Special Issue, we welcome original research and review articles that provide an overview of this topic.

Dr. Silvia Peppicelli
Dr. Elena Andreucci
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.

Published Papers (1 paper)

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Research

18 pages, 2495 KiB  
Article
Lactococcus lactis subsp. cremoris C60 Upregulates Macrophage Function by Modifying Metabolic Preference in Enhanced Anti-Tumor Immunity
by Suguru Saito, Duo-Yao Cao, Toshio Maekawa, Noriko M. Tsuji and Alato Okuno
Cancers 2024, 16(10), 1928; https://doi.org/10.3390/cancers16101928 - 18 May 2024
Viewed by 282
Abstract
Lactococcus lactis subsp. cremoris C60 is a probiotic strain of lactic acid bacteria (LAB) which induces various immune modifications in myeloid lineage cells. These modifications subsequently regulate T cell function, resulting in enhanced immunity both locally and systemically. Here, we report that C60 [...] Read more.
Lactococcus lactis subsp. cremoris C60 is a probiotic strain of lactic acid bacteria (LAB) which induces various immune modifications in myeloid lineage cells. These modifications subsequently regulate T cell function, resulting in enhanced immunity both locally and systemically. Here, we report that C60 suppresses tumor growth by enhancing macrophage function via metabolic alterations, thereby increasing adenosine triphosphate (ATP) production in a murine melanoma model. Intragastric (i.g.) administration of C60 significantly reduced tumor volume compared to saline administration in mice. The anti-tumor function of intratumor (IT) macrophage was upregulated in mice administered with C60, as evidenced by an increased inflammatory phenotype (M1) rather than an anti-inflammatory/reparative (M2) phenotype, along with enhanced antigen-presenting ability, resulting in increased tumor antigen-specific CD8+ T cells. Through this functional modification, we identified that C60 establishes a glycolysis-dominant metabolism, rather than fatty acid oxidation (FAO), in IT macrophages, leading to increased intracellular ATP levels. To address the question of why orally supplemented C60 exhibits functions in distal places, we found a possibility that bacterial cell wall components, which could be distributed throughout the body from the gut, may induce stimulatory signals in peripheral macrophages via Toll-like receptors (TLRs) signaling activation. Thus, C60 strengthens macrophage anti-tumor immunity by promoting a predominant metabolic shift towards glycolysis upon TLR-mediated stimulation, thereby increasing substantial energy production. Full article
(This article belongs to the Special Issue Advances in Acidosis within the Tumor Microenvironment)
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