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Cells
Special Issues
Tumor Microenvironment and Cancer Cells—Key Interactions in Cancer Progression
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Tumor Microenvironment and Cancer Cells—Key Interactions in Cancer Progression

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (15 December 2021) | Viewed by 15275

Special Issue Editors

Prof. Dr. Piotr Dziegiel

E-Mail Website
Guest Editor
Department of Histology and Embryology, Department of Human Morphology and Embryology, Wroclaw Medical University, Chałubińskiego 6a St, 50-368 Wrocław, Poland
Interests: cancer biology; cell proliferation; cancer biomarkers; tumor microenvironment; immunohistochemistry; histology
Special Issues, Collections and Topics in MDPI journals
Dr. Karolina Jablonska

E-Mail Website
Assistant Guest Editor
Department of Histology and Embryology, Department of Human Morphology and Embryology, Wroclaw Medical University, Chałubińskiego 6a St, 50-368 Wrocław, Poland
Interests: cancer biology; cell proliferation; cancer biomarkers; tumor microenvironment; immunohistochemistry; histology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Tumor development and progression, as well as the tumor response to different types of treatment, are the result of the continuous crosstalk between cancer cells and the tumor microenvironment (TME). The TME is an important player influencing the growth of cancers and impacting the outcomes of therapy. TME properties such as hypoxia, oxidative stress and acidosis are linked to increased tumor aggressiveness and treatment resistance. Additionally, cytokines and growth factors secreted by the tumor microenvironment, stroma crosstalk, changes in metabolism, and innate and adaptive immune responses affect the epithelial-to-mesenchymal transition (EMT) process. Changes in the extracellular environment of the tumor affect miRNAs, which play an important role in the control of the malignant behavior of cancer cells. TME components such as cancer-associated fibroblasts (CAFs), extracellular matrix (ECM) proteins, cancer stem cells (CSCs), different signaling molecules, proinflammatory factors and immune cells interact with one another, being promising therapeutic targets. Recent cancer studies described exosomes secreted by TME cells as messengers modulating the tumor environment to facilitate tumor progression. In this Special Issue, we will discuss tumor biology, the composition of the TME, its prognostic and predictive value and therapeutic strategies targeting TME components.

Prof. Piotr Dziegiel
Dr. Karolina Jablonska
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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
  • tumor microenvironment
  • extracellular matrix
  • cancer-associated fibroblasts
  • cancer stem cells
  • hypoxia
  • immune response
  • exosomes

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Published Papers (4 papers)

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Research

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22 pages, 4308 KiB  
Article
Dermatan Sulfate Affects Breast Cancer Cell Function via the Induction of Necroptosis
by Grzegorz Wisowski, Adam Pudełko, Krystyna Olczyk, Monika Paul-Samojedny and Ewa M. Koźma
Cells 2022, 11(1), 173; https://doi.org/10.3390/cells11010173 - 5 Jan 2022
Cited by 6 | Viewed by 2394
Abstract
Dermatan sulfate (DS) is widespread in the extracellular matrix (ECM) of animal tissues. This glycosaminoglycan is characterized by a variable structure, which is reflected in the heterogeneity of its sulfation pattern. The sulfate groups are responsible for the binding properties of DS, which [...] Read more.
Dermatan sulfate (DS) is widespread in the extracellular matrix (ECM) of animal tissues. This glycosaminoglycan is characterized by a variable structure, which is reflected in the heterogeneity of its sulfation pattern. The sulfate groups are responsible for the binding properties of DS, which determine an interaction profile of this glycan. However, the detailed role of DS in biological processes such as the neoplasm is still poorly understood. The aim of the study was to assess the effects of the structural variants of DS on breast cancer cells. We found that DS isoforms from normal and fibrotic fascia as well as from intestinal mucosa were able to quickly induce oxidative stress in the cytoplasm and affect the mitochondrial function in luminal breast cancer cells. Moreover, the variants caused the necroptosis of the cells most likely via the first of these mechanisms. This death was responsible for a reduction in the viability and number of breast cancer cells. However, the dynamics and intensity of all of the DS variants-triggered effects were strongly dependent on the cell type and the structure of these molecules. The most pronounced activity was demonstrated by those variants that shared structural features with the DS from the tumor niche. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Cancer Cells—Key Interactions in Cancer Progression)
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17 pages, 6920 KiB  
Article
Targeting Chondroitin Sulfate Reduces Invasiveness of Glioma Cells by Suppressing CD44 and Integrin β1 Expression
by Yin-Hung Chu, Wen-Chieh Liao, Ying-Jui Ho, Chih-Hsien Huang, To-Jung Tseng and Chiung-Hui Liu
Cells 2021, 10(12), 3594; https://doi.org/10.3390/cells10123594 - 20 Dec 2021
Cited by 17 | Viewed by 4625
Abstract
Chondroitin sulfate (CS) is a major component of the extracellular matrix found to be abnormally accumulated in several types of cancer tissues. Previous studies have indicated that CS synthases and modification enzymes are frequently elevated in human gliomas and are associated with poor [...] Read more.
Chondroitin sulfate (CS) is a major component of the extracellular matrix found to be abnormally accumulated in several types of cancer tissues. Previous studies have indicated that CS synthases and modification enzymes are frequently elevated in human gliomas and are associated with poor prognosis. However, the underlying mechanisms of CS in cancer progression and approaches for interrupting its functions in cancer cells remain largely unexplored. Here, we have found that CS was significantly enriched surrounding the vasculature in a subset of glioma tissues, which was akin to the perivascular niche for cancer-initiating cells. Silencing or overexpression of the major CS synthase, chondroitin sulfate synthase 1 (CHSY1), significantly regulated the glioma cell invasive phenotypes and modulated integrin expression. Furthermore, we identified CD44 as a crucial chondroitin sulfate proteoglycan (CSPG) that was modified by CHSY1 on glioma cells, and the suppression of CS formation on CD44 by silencing the CHSY1-inhibited interaction between CD44 and integrin β1 on the adhesion complex. Moreover, we tested the CS-specific binding peptide, resulting in the suppression of glioma cell mobility in a fashion similar to that observed upon the silencing of CHSY1. In addition, the peptide demonstrated significant affinity to CD44, promoted CD44 degradation, and suppressed integrin β1 expression in glioma cells. Overall, this study proposes a potential regulatory loop between CS, CD44, and integrin β1 in glioma cells, and highlights the importance of CS in CD44 stability. Furthermore, the targeting of CS by specific binding peptides has potential as a novel therapeutic strategy for glioma. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Cancer Cells—Key Interactions in Cancer Progression)
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18 pages, 1409 KiB  
Article
Combination of GP88 Expression in Tumor Cells and Tumor-Infiltrating Immune Cells Is an Independent Prognostic Factor for Bladder Cancer Patients
by Markus Eckstein, Verena Lieb, Rudolf Jung, Danijel Sikic, Katrin Weigelt, Robert Stöhr, Carol Geppert, Veronika Weyerer, Simone Bertz, Ginette Serrero, Binbin Yue, Arndt Hartmann, Bernd Wullich, Helge Taubert and Sven Wach
Cells 2021, 10(7), 1796; https://doi.org/10.3390/cells10071796 - 15 Jul 2021
Cited by 3 | Viewed by 2618
Abstract
Urothelial bladder cancer (BCa) is the ninth most commonly diagnosed cancer worldwide and accounts for approximately 3% of global cancer diagnoses. We are interested in prognostic markers that may characterize tumor cells (TCs) and immune cells (ICs) and their relationship in BCa. A [...] Read more.
Urothelial bladder cancer (BCa) is the ninth most commonly diagnosed cancer worldwide and accounts for approximately 3% of global cancer diagnoses. We are interested in prognostic markers that may characterize tumor cells (TCs) and immune cells (ICs) and their relationship in BCa. A potential candidate marker that meets these criteria is progranulin (GP88), which is expressed separately in TCs and ICs. We analyzed GP88 expression by immunohistochemistry (IHC) in 196 muscle-invasive BCa samples using a tissue microarray. The immunoreactive score for GP88 staining in TCs and the percentage of GP88-positive ICs was determined. An easy cutoff for the staining status of TCs (positive vs. negative) and ICs (0% vs. >0%) and, more generally, negative vs. positive GP88 staining could be applied. We detected 93 patients (47.4%) and 92 patients (46.9%) with GP88-positive TCs or ICs, respectively. The IHC results were correlated with clinicopathological and survival data. Positive GP88 staining in TCs appeared to be an independent poor prognostic factor for disease-specific survival (DSS) (RR (relative risk) = 1.74; p = 0.009) and recurrence-free survival (RFS) (RR = 1.92; p = 0.002). In contrast, negative GP88 staining in ICs was an independent negative predictor for overall survival (OS) (RR = 2.18; p < 0.001), DSS (RR = 2.84; p < 0.001) and RFS (RR = 2.91; p < 0.001) in multivariate Cox’s regression analysis. When combining GP88 staining in TCs and ICs, a specific combination of GP88-positive TCs and GP88-negative ICs was associated with a 2.54-fold increased risk of death, a 4.21-fold increased risk of disease-specific death and a 4.81-fold increased risk of recurrence compared to GP88-negative TCs and GP88-positive ICs. In summary, GP88 positivity in TCs is a negative prognostic factor for DSS and RFS. In addition, GP88 positivity can mark ICs that are associated with a good prognosis (OS, DSS and RFS). The combination of GP88 staining in TCs and ICs appears to be a significant independent prognostic biomarker in muscle-invasive BCa. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Cancer Cells—Key Interactions in Cancer Progression)
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Review

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22 pages, 1943 KiB  
Review
The Role of Irisin in Cancer Disease
by Agnieszka Pinkowska, Marzenna Podhorska-Okołów, Piotr Dzięgiel and Katarzyna Nowińska
Cells 2021, 10(6), 1479; https://doi.org/10.3390/cells10061479 - 12 Jun 2021
Cited by 28 | Viewed by 4613
Abstract
Irisin (Ir) is an adipomyokine that is involved in the regulation of metabolic processes. It also influences processes related to inflammation, including cancer. Initially, Ir was considered a hormone secreted by skeletal muscles in response to physical exercise. Further studies showed that Ir [...] Read more.
Irisin (Ir) is an adipomyokine that is involved in the regulation of metabolic processes. It also influences processes related to inflammation, including cancer. Initially, Ir was considered a hormone secreted by skeletal muscles in response to physical exercise. Further studies showed that Ir is also present in other healthy tissues, organs, and plasma. It influences the change in phenotype of white adipose tissue (WAT) into brown adipose tissue (BAT). It increases mitochondrial biogenesis and affects the expression of thermogenin (UCP1). This adipomyokine has also been found in many tumor tissues and in the serum of cancer patients. Studies are underway to determine the association between Ir and carcinogenesis. It has been confirmed that Ir inhibits in vitro proliferation, migration, and invasion. It is involved in the inhibition of epithelial–mesenchymal transition (EMT). Additionally, Ir affects the expression of the transcription factor Snail, which is involved in EMT, and inhibits transcription of the gene encoding E-cadherin, which is characteristic of epithelial-derived cells. Many studies have been performed to determine the role of Ir in physiological and pathological processes. Further detailed studies should determine more precisely the effect of Ir on the body in health and disease. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Cancer Cells—Key Interactions in Cancer Progression)
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