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Advances in Tumor Microenvironment and Metabolism

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 (30 June 2023) | Viewed by 2270

Special Issue Editor

Department of Food Science and Biotechnology, Kyungpook National University, Daegu 41566, Republic of Korea
Interests: tumor microenvironment; obesity; cell signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The tumor microenvironment has profound effects on cancer development, progression, and treatment response. Cancer cells coexist with infiltrated immune cells, blood vessels, fibroblasts, and other stromal cells in the tumor microenvironment. Additionally, the biochemical and biophysical properties of the tumor microenvironment are different from those of normal tissue. Several features of the tumor microenvironment have been identified, including hypoxia, acidosis, high interstitial fluid pressure, and increased extracellular matrix (ECM) stiffness. The metabolism of cancer cells is reprogrammed from that of normal cells. The glycolytic metabolism of cacti produces lactic acid, which, after being excreted by cancer cells, can acidify the tumor microenvironment. Additionally, tumor-associated hypoxia can lead to rapid cancer growth, and defective vascular perfusion can further increase cellular glycolysis as well as lactate production and accumulation in the tumor microenvironment. Cancer cell metabolism is being exploited as a target for cancer therapy. This Special Issue will address several aspects of the tumor microenvironment and metabolism. Despite considerable research progress, the complex interplay between cancer cells, metabolism, and the tumor microenvironment is still not fully understood, and we would like to provide open source sharing that may enhance our understanding.

Dr. Ju-Ock Nam
Guest Editor

Manuscript Submission Information

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Keywords

  • vasculature
  • hypoxia
  • carcinoma-associated fibroblast
  • extracellular matrix protein
  • immune cells
  • tumor-cell mitochondria
  • glycolysis
  • metabolic reprogramming
  • lactic acidosis
  • cancer chachexia

Published Papers (1 paper)

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Research

15 pages, 14403 KiB  
Article
MUC1 Expression Affects the Immunoflogosis in Renal Cell Carcinoma Microenvironment through Complement System Activation and Immune Infiltrate Modulation
by Giuseppe Lucarelli, Giuseppe Stefano Netti, Monica Rutigliano, Francesco Lasorsa, Davide Loizzo, Martina Milella, Annalisa Schirinzi, Antonietta Fontana, Francesca Di Serio, Roberto Tamma, Domenico Ribatti, Michele Battaglia, Elena Ranieri and Pasquale Ditonno
Int. J. Mol. Sci. 2023, 24(5), 4814; https://doi.org/10.3390/ijms24054814 - 02 Mar 2023
Cited by 26 | Viewed by 2016
Abstract
Mucin1 (MUC1), a glycoprotein associated with an aggressive cancer phenotype and chemoresistance, is aberrantly overexpressed in a subset of clear cell renal cell carcinoma (ccRCC). Recent studies suggest that MUC1 plays a role in modulating cancer cell metabolism, but its role in regulating [...] Read more.
Mucin1 (MUC1), a glycoprotein associated with an aggressive cancer phenotype and chemoresistance, is aberrantly overexpressed in a subset of clear cell renal cell carcinoma (ccRCC). Recent studies suggest that MUC1 plays a role in modulating cancer cell metabolism, but its role in regulating immunoflogosis in the tumor microenvironment remains poorly understood. In a previous study, we showed that pentraxin-3 (PTX3) can affect the immunoflogosis in the ccRCC microenvironment by activating the classical pathway of the complement system (C1q) and releasing proangiogenic factors (C3a, C5a). In this scenario, we evaluated the PTX3 expression and analyzed the potential role of complement system activation on tumor site and immune microenvironment modulation, stratifying samples in tumors with high (MUC1H) versus tumors with low MUC1 expression (MUC1L). We found that PTX3 tissue expression was significantly higher in MUC1H ccRCC. In addition, C1q deposition and the expressions of CD59, C3aR, and C5aR were extensively present in MUC1H ccRCC tissue samples and colocalized with PTX3. Finally, MUC1 expression was associated with an increased number of infiltrating mast cells, M2-macrophage, and IDO1+ cells, and a reduced number of CD8+ T cells. Taken together, our results suggest that expression of MUC1 can modulate the immunoflogosis in the ccRCC microenvironment by activating the classical pathway of the complement system and regulating the immune infiltrate, promoting an immune-silent microenvironment. Full article
(This article belongs to the Special Issue Advances in Tumor Microenvironment and Metabolism)
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