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Tumor Microenvironment: Cellular Interaction and Metabolic Adaptations
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Tumor Microenvironment: Cellular Interaction and Metabolic Adaptations

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 21475

Special Issue Editors

Dr. Chiara Focaccetti

E-Mail Website
Guest Editor
Department of Clinical Sciences and Translational Medicine, Università degli Studi di Roma “Tor Vergata”, Via Montpellier, 1, 00133 Roma, Italy
Interests: T-cell response in cancer; cancer vaccines; cancer immunotherapy; preclinical models of cancer; natural compounds and cancer
Dr. Monica Benvenuto

E-Mail Website
Guest Editor
1. Departmental Faculty of Medicine and Surgery, Saint Camillus International University of Health and Medical Sciences, Via di Sant’Alessandro 8, 00131 Rome, Italy
2. Department of Clinical Sciences and Translational Medicine, Università degli Studi di Roma “Tor Vergata”, Via Montpellier, 1, 00133 Rome, Italy
Interests: cancer cell lines; polyphenols; dietary compounds and cancer; cancer immunotherapy; cancer treatment in animal models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The tumor microenvironment (TME) plays a critical role in cancerogenesis. Different components of the TME (such as cancer cells, cancer-associated fibroblasts, endothelial cells, tumor-infiltrating immune cells, adipocytes, and the extracellular matrix (ECM)) influence the development and progression of cancer, the adaptation of cancer cells and their resistance to anti-cancer therapies. In addition, metabolic factors, such as hypoxia and inflammation, determine the formation of a tumor-supportive microenvironment. The development of anticancer approaches aimed at remodeling the TME is very promising.

This Special Issue focuses on the role of the TME in cancer development and progression and on new therapeutic approaches for the treatment of metastatic tumors through TME remodeling. The metabolic flexibility of cancer cells and their ability to adapt to changes in nutrient availability is also an interesting topic that deserves further attention. The interaction between cancer cells and cells of the immune system constantly needs revision because new phenotypes are frequently being described.

Therefore, submissions of original research articles or reviews related to the impact of the TME on cancer progression, the metabolic plasticity of cancerous and non-cancerous cells, and therapeutic strategies for remodeling these various aspects in cancer are encouraged. 

Dr. Chiara Focaccetti
Dr. Monica Benvenuto
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • tumor microenvironment
  • stromal cells
  • immune cells
  • tumor metabolism
  • hypoxia
  • inflammation

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Published Papers (6 papers)

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Editorial

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4 pages, 172 KiB  
Editorial
Tumor Microenvironment: Cellular Interaction and Metabolic Adaptations
by Monica Benvenuto and Chiara Focaccetti
Int. J. Mol. Sci. 2024, 25(7), 3642; https://doi.org/10.3390/ijms25073642 - 25 Mar 2024
Viewed by 920
Abstract
The tumor microenvironment (TME) plays a critical role in cancerogenesis [...] Full article
(This article belongs to the Special Issue Tumor Microenvironment: Cellular Interaction and Metabolic Adaptations)

Research

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16 pages, 4319 KiB  
Article
Fat Loss in Patients with Metastatic Clear Cell Renal Cell Carcinoma Treated with Immune Checkpoint Inhibitors
by Ji Hyun Lee, Soohyun Hwang, ByulA Jee, Jae-Hun Kim, Jihwan Lee, Jae Hoon Chung, Wan Song, Hyun Hwan Sung, Hwang Gyun Jeon, Byong Chang Jeong, Seong Il Seo, Seong Soo Jeon, Hyun Moo Lee, Se Hoon Park, Ghee Young Kwon and Minyong Kang
Int. J. Mol. Sci. 2023, 24(4), 3994; https://doi.org/10.3390/ijms24043994 - 16 Feb 2023
Viewed by 1817
Abstract
The purpose of this study was to determine the prognostic impact of fat loss after immune checkpoint inhibitor (ICI) treatment in patients with metastatic clear cell renal cell carcinoma (ccRCC). Data from 60 patients treated with ICI therapy for metastatic ccRCC were retrospectively [...] Read more.
The purpose of this study was to determine the prognostic impact of fat loss after immune checkpoint inhibitor (ICI) treatment in patients with metastatic clear cell renal cell carcinoma (ccRCC). Data from 60 patients treated with ICI therapy for metastatic ccRCC were retrospectively analyzed. Changes in cross-sectional areas of subcutaneous fat (SF) between the pre-treatment and post-treatment abdominal computed tomography (CT) images were expressed as percentages and were divided by the interval between the CT scans to calculate ΔSF (%/month). SF loss was defined as ΔSF < −5%/month. Survival analyses for overall survival (OS) and progression-free survival (PFS) were performed. Patients with SF loss had shorter OS (median, 9.5 months vs. not reached; p < 0.001) and PFS (median, 2.6 months vs. 33.5 months; p < 0.001) than patients without SF loss. ΔSF was independently associated with OS (adjusted hazard ratio (HR), 1.49; 95% confidence interval (CI), 1.07–2.07; p = 0.020) and PFS (adjusted HR, 1.57; 95% CI, 1.17–2.12; p = 0.003), with a 5%/month decrease in SF increasing the risk of death and progression by 49% and 57%, respectively. In conclusion, Loss of SF after treatment initiation is a significant and independent poor prognostic factor for OS and PFS in patients with metastatic ccRCC who receive ICI therapy. Full article
(This article belongs to the Special Issue Tumor Microenvironment: Cellular Interaction and Metabolic Adaptations)
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Review

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21 pages, 3069 KiB  
Review
Therapeutic Potential of Tumor Metabolic Reprogramming in Triple-Negative Breast Cancer
by Gyöngyi Munkácsy, Libero Santarpia and Balázs Győrffy
Int. J. Mol. Sci. 2023, 24(8), 6945; https://doi.org/10.3390/ijms24086945 - 8 Apr 2023
Cited by 11 | Viewed by 3927
Abstract
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, with clinical features of high metastatic potential, susceptibility to relapse, and poor prognosis. TNBC lacks the expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor [...] Read more.
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, with clinical features of high metastatic potential, susceptibility to relapse, and poor prognosis. TNBC lacks the expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). It is characterized by genomic and transcriptional heterogeneity and a tumor microenvironment (TME) with the presence of high levels of stromal tumor-infiltrating lymphocytes (TILs), immunogenicity, and an important immunosuppressive landscape. Recent evidence suggests that metabolic changes in the TME play a key role in molding tumor development by impacting the stromal and immune cell fractions, TME composition, and activation. Hence, a complex inter-talk between metabolic and TME signaling in TNBC exists, highlighting the possibility of uncovering and investigating novel therapeutic targets. A better understanding of the interaction between the TME and tumor cells, and the underlying molecular mechanisms of cell–cell communication signaling, may uncover additional targets for better therapeutic strategies in TNBC treatment. In this review, we aim to discuss the mechanisms in tumor metabolic reprogramming, linking these changes to potential targetable molecular mechanisms to generate new, physical science-inspired clinical translational insights for the cure of TNBC. Full article
(This article belongs to the Special Issue Tumor Microenvironment: Cellular Interaction and Metabolic Adaptations)
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17 pages, 8435 KiB  
Review
Hypoxia in Skin Cancer: Molecular Basis and Clinical Implications
by Sungmi Jeon, Miyeon Jeon, Sanga Choi, Seongkyeong Yoo, Soohyun Park, Mingyu Lee and Iljin Kim
Int. J. Mol. Sci. 2023, 24(5), 4430; https://doi.org/10.3390/ijms24054430 - 23 Feb 2023
Cited by 7 | Viewed by 3628
Abstract
Skin cancer is one of the most prevalent cancers in the Caucasian population. In the United States, it is estimated that at least one in five people will develop skin cancer in their lifetime, leading to significant morbidity and a healthcare burden. Skin [...] Read more.
Skin cancer is one of the most prevalent cancers in the Caucasian population. In the United States, it is estimated that at least one in five people will develop skin cancer in their lifetime, leading to significant morbidity and a healthcare burden. Skin cancer mainly arises from cells in the epidermal layer of the skin, where oxygen is scarce. There are three main types of skin cancer: malignant melanoma, basal cell carcinoma, and squamous cell carcinoma. Accumulating evidence has revealed a critical role for hypoxia in the development and progression of these dermatologic malignancies. In this review, we discuss the role of hypoxia in treating and reconstructing skin cancers. We will summarize the molecular basis of hypoxia signaling pathways in relation to the major genetic variations of skin cancer. Full article
(This article belongs to the Special Issue Tumor Microenvironment: Cellular Interaction and Metabolic Adaptations)
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42 pages, 1744 KiB  
Review
Autophagy and the Insulin-like Growth Factor (IGF) System in Colonic Cells: Implications for Colorectal Neoplasia
by Aldona Kasprzak
Int. J. Mol. Sci. 2023, 24(4), 3665; https://doi.org/10.3390/ijms24043665 - 11 Feb 2023
Cited by 8 | Viewed by 5398
Abstract
Colorectal cancer (CRC) is one of the most common human malignancies worldwide. Along with apoptosis and inflammation, autophagy is one of three important mechanisms in CRC. The presence of autophagy/mitophagy in most normal mature intestinal epithelial cells has been confirmed, where it has [...] Read more.
Colorectal cancer (CRC) is one of the most common human malignancies worldwide. Along with apoptosis and inflammation, autophagy is one of three important mechanisms in CRC. The presence of autophagy/mitophagy in most normal mature intestinal epithelial cells has been confirmed, where it has mainly protective functions against reactive oxygen species (ROS)-induced DNA and protein damage. Autophagy regulates cell proliferation, metabolism, differentiation, secretion of mucins and/or anti-microbial peptides. Abnormal autophagy in intestinal epithelial cells leads to dysbiosis, a decline in local immunity and a decrease in cell secretory function. The insulin-like growth factor (IGF) signaling pathway plays an important role in colorectal carcinogenesis. This is evidenced by the biological activities of IGFs (IGF-1 and IGF-2), IGF-1 receptor type 1 (IGF-1R) and IGF-binding proteins (IGF BPs), which have been reported to regulate cell survival, proliferation, differentiation and apoptosis. Defects in autophagy are found in patients with metabolic syndrome (MetS), inflammatory bowel diseases (IBD) and CRC. In neoplastic cells, the IGF system modulates the autophagy process bidirectionally. In the current era of improving CRC therapies, it seems important to investigate the exact mechanisms not only of apoptosis, but also of autophagy in different populations of tumor microenvironment (TME) cells. The role of the IGF system in autophagy in normal as well as transformed colorectal cells still seems poorly understood. Hence, the aim of the review was to summarize the latest knowledge on the role of the IGF system in the molecular mechanisms of autophagy in the normal colon mucosa and in CRC, taking into account the cellular heterogeneity of the colonic and rectal epithelium. Full article
(This article belongs to the Special Issue Tumor Microenvironment: Cellular Interaction and Metabolic Adaptations)
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21 pages, 1743 KiB  
Review
Glutamine Metabolism in Cancer Stem Cells: A Complex Liaison in the Tumor Microenvironment
by Francesco Pacifico, Antonio Leonardi and Elvira Crescenzi
Int. J. Mol. Sci. 2023, 24(3), 2337; https://doi.org/10.3390/ijms24032337 - 25 Jan 2023
Cited by 12 | Viewed by 5089
Abstract
In this review we focus on the role of glutamine in control of cancer stem cell (CSC) fate. We first provide an overview of glutamine metabolism, and then summarize relevant studies investigating how glutamine metabolism modulates the CSC compartment, concentrating on solid tumors. [...] Read more.
In this review we focus on the role of glutamine in control of cancer stem cell (CSC) fate. We first provide an overview of glutamine metabolism, and then summarize relevant studies investigating how glutamine metabolism modulates the CSC compartment, concentrating on solid tumors. We schematically describe how glutamine in CSC contributes to several metabolic pathways, such as redox metabolic pathways, ATP production, non-essential aminoacids and nucleotides biosynthesis, and ammonia production. Furthermore, we show that glutamine metabolism is a key regulator of epigenetic modifications in CSC. Finally, we briefly discuss how cancer-associated fibroblasts, adipocytes, and senescent cells in the tumor microenvironment may indirectly influence CSC fate by modulating glutamine availability. We aim to highlight the complexity of glutamine’s role in CSC, which supports our knowledge about metabolic heterogeneity within the CSC population. Full article
(This article belongs to the Special Issue Tumor Microenvironment: Cellular Interaction and Metabolic Adaptations)
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