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Cancers
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Molecular Mechanisms of Cancer: Focus on Metabolism and Microenvironment
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Molecular Mechanisms of Cancer: Focus on Metabolism and Microenvironment

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

Deadline for manuscript submissions: closed (28 November 2022) | Viewed by 16167

Special Issue Editor

Dr. Laetitia Linares

E-Mail Website
Guest Editor
NSERM, Institut National de la Santé et de la Recherche Médicale, Paris, France
Interests: cancer; molecular mechanism; gene expression; microenvironment; metabolism

Special Issue Information

Dear Colleagues,

The impact of cancer cells on their environment (both locally and distantly) is known to promote malignancy and chemoresistance. Cancers are not just composed of malignant cells but are a complex mass to which many other cells are recruited; this process can contribute to cell transformation. Interactions between transformed and non-malignant cells represent the tumor microenvironment (TME). Intercellular communication is driven by a complex and dynamic metabolism. Moreover, metabolism is a hallmark of cancer and a critical target for cancer therapy. Cancer metabolism is regulated by the autonomous mechanism of the cell as well as metabolite availability in the TME.

Understanding the interactions between the cancer cell and environmental metabolism will be critical for combining metabolism-targeted therapies with chemotherapies. It is known that cancer cells compete with T cells for glucose in tumors and that restricting T cell glucose metabolism causes lymphocyte exhaustion. Other nutrient levels can affect both cancer and immune cells. The relationship between tumors and other organ systems is not limited to the immune system. Endothelial cells also undergo factor-induced metabolic reprogramming. Cancer also causes alterations in whole-body metabolism that may influence tumor-nutrient availability. Modulating the amino acid composition of the diet can slow cancer growth, and investigation into how diet affects tumor growth remains an underexplored area.

Different studies suggest that targeting the metabolism involved in the communication between the non-malignant cells and the malignant cells could be a new treatment option.

Dr. Laetitia Linares
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 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
  • malignancy
  • chemoresistance
  • tumor microenvironment
  • targeting metabolism
  • cancer growth
  • non-malignant cells
  • malignant cells

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Published Papers (4 papers)

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35 pages, 3727 KiB  
Review
Tumor Microenvironment Features and Chemoresistance in Pancreatic Ductal Adenocarcinoma: Insights into Targeting Physicochemical Barriers and Metabolism as Therapeutic Approaches
by Tiago M. A. Carvalho, Daria Di Molfetta, Maria Raffaella Greco, Tomas Koltai, Khalid O. Alfarouk, Stephan J. Reshkin and Rosa A. Cardone
Cancers 2021, 13(23), 6135; https://doi.org/10.3390/cancers13236135 - 6 Dec 2021
Cited by 36 | Viewed by 5127
Abstract
Currently, the median overall survival of PDAC patients rarely exceeds 1 year and has an overall 5-year survival rate of about 9%. These numbers are anticipated to worsen in the future due to the lack of understanding of the factors involved in its [...] Read more.
Currently, the median overall survival of PDAC patients rarely exceeds 1 year and has an overall 5-year survival rate of about 9%. These numbers are anticipated to worsen in the future due to the lack of understanding of the factors involved in its strong chemoresistance. Chemotherapy remains the only treatment option for most PDAC patients; however, the available therapeutic strategies are insufficient. The factors involved in chemoresistance include the development of a desmoplastic stroma which reprograms cellular metabolism, and both contribute to an impaired response to therapy. PDAC stroma is composed of immune cells, endothelial cells, and cancer-associated fibroblasts embedded in a prominent, dense extracellular matrix associated with areas of hypoxia and acidic extracellular pH. While multiple gene mutations are involved in PDAC initiation, this desmoplastic stroma plays an important role in driving progression, metastasis, and chemoresistance. Elucidating the mechanisms underlying PDAC resistance are a prerequisite for designing novel approaches to increase patient survival. In this review, we provide an overview of the stromal features and how they contribute to the chemoresistance in PDAC treatment. By highlighting new paradigms in the role of the stromal compartment in PDAC therapy, we hope to stimulate new concepts aimed at improving patient outcomes. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer: Focus on Metabolism and Microenvironment)
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20 pages, 2756 KiB  
Review
Cancer-Associated Fibroblast Diversity Shapes Tumor Metabolism in Pancreatic Cancer
by Raphaël Peiffer, Yasmine Boumahd, Charlotte Gullo, Rebekah Crake, Elisabeth Letellier, Akeila Bellahcène and Olivier Peulen
Cancers 2023, 15(1), 61; https://doi.org/10.3390/cancers15010061 - 22 Dec 2022
Cited by 11 | Viewed by 4574
Abstract
Despite extensive research, the 5-year survival rate of pancreatic cancer (PDAC) patients remains at only 9%. Patients often show poor treatment response, due partly to a highly complex tumor microenvironment (TME). Cancer-associated fibroblast (CAF) heterogeneity is characteristic of the pancreatic TME, where several [...] Read more.
Despite extensive research, the 5-year survival rate of pancreatic cancer (PDAC) patients remains at only 9%. Patients often show poor treatment response, due partly to a highly complex tumor microenvironment (TME). Cancer-associated fibroblast (CAF) heterogeneity is characteristic of the pancreatic TME, where several CAF subpopulations have been identified, such as myofibroblastic CAFs (myCAFs), inflammatory CAFs (iCAFs), and antigen presenting CAFs (apCAFs). In PDAC, cancer cells continuously adapt their metabolism (metabolic switch) to environmental changes in pH, oxygenation, and nutrient availability. Recent advances show that these environmental alterations are all heavily driven by stromal CAFs. CAFs and cancer cells exchange cytokines and metabolites, engaging in a tight bidirectional crosstalk, which promotes tumor aggressiveness and allows constant adaptation to external stress, such as chemotherapy. In this review, we summarize CAF diversity and CAF-mediated metabolic rewiring, in a PDAC-specific context. First, we recapitulate the most recently identified CAF subtypes, focusing on the cell of origin, activation mechanism, species-dependent markers, and functions. Next, we describe in detail the metabolic crosstalk between CAFs and tumor cells. Additionally, we elucidate how CAF-driven paracrine signaling, desmoplasia, and acidosis orchestrate cancer cell metabolism. Finally, we highlight how the CAF/cancer cell crosstalk could pave the way for new therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer: Focus on Metabolism and Microenvironment)
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10 pages, 834 KiB  
Perspective
The Prime and Integral Cause of Cancer in the Post-Warburg Era
by Salvador Harguindey, Stephan J. Reshkin and Khalid O. Alfarouk
Cancers 2023, 15(2), 540; https://doi.org/10.3390/cancers15020540 - 16 Jan 2023
Viewed by 3189
Abstract
Back to beginnings. A century ago, Otto Warburg published that aerobic glycolysis and the respiratory impairment of cells were the prime cause of cancer, a phenomenon that since then has been known as “the Warburg effect”. In his early studies, Warburg looked at [...] Read more.
Back to beginnings. A century ago, Otto Warburg published that aerobic glycolysis and the respiratory impairment of cells were the prime cause of cancer, a phenomenon that since then has been known as “the Warburg effect”. In his early studies, Warburg looked at the effects of hydrogen ions (H+), on glycolysis in anaerobic conditions, as well as of bicarbonate and glucose. He found that gassing with CO2 led to the acidification of the solutions, resulting in decreased rates of glycolysis. It appears that Warburg first interpreted the role of pH on glycolysis as a secondary phenomenon, a side effect that was there just to compensate for the effect of bicarbonate. However, later on, while talking about glycolysis in a seminar at the Rockefeller Foundation, he said: “Special attention should be drawn to the remarkable influence of the bicarbonate…”. Departing from the very beginnings of this metabolic cancer research in the 1920s, our perspective advances an analytic as well as the synthetic approach to the new “pH-related paradigm of cancer”, while at the same time addressing the most fundamental and recent changing concepts in cancer metabolic etiology and its potential therapeutic implications. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer: Focus on Metabolism and Microenvironment)
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20 pages, 9512 KiB  
Article
Inhibition of IDH3α Enhanced the Efficacy of Chemoimmunotherapy by Regulating Acidic Tumor Microenvironments
by Lingling Zhang, Yang Song, Xiaoyan Dai, Wenwen Xu, Mengxia Li and Yuxi Zhu
Cancers 2023, 15(6), 1802; https://doi.org/10.3390/cancers15061802 - 16 Mar 2023
Viewed by 2156
Abstract
In recent years, chemoimmunotherapy has become effective in some advanced cancers, but its effect is still limited. Transcriptional upregulation of isocitrate dehydrogenase 3α (IDH3α) can promote tumor initiation and progression. However, it is not clear whether the aberrant expression of IDH3α is related [...] Read more.
In recent years, chemoimmunotherapy has become effective in some advanced cancers, but its effect is still limited. Transcriptional upregulation of isocitrate dehydrogenase 3α (IDH3α) can promote tumor initiation and progression. However, it is not clear whether the aberrant expression of IDH3α is related to the efficacy of chemoimmunotherapy in cancers. Here, we found that IDH3α was elevated in uterine cervical cancer (UCC) and lung adenocarcinoma (LUAD) samples by using public databases. High expression of IDH3α could promote the epithelial–mesenchymal transition (EMT), alter the intracellular redox status, promote glycolysis, and induce an acidic microenvironments in cancer cells. Furthermore, we found that inhibition of IDH3α combined with chemoimmunotherapy (cisplatin and programmed cell death ligand 1 (PD-L1) antibodies) activated the cGAS–STING pathway, promoted CD8+ T cell infiltration, and decreased tumor growth in mouse models of cervical cancer. In conclusion, our data indicate that silencing IDH3α sensitizes tumors to chemoimmunotherapy by modulating the acidic microenvironment and activating the cGAS–STING pathway. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer: Focus on Metabolism and Microenvironment)
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