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Brain Tumors and Their Microenvironment: Focus on Hypoxia, Oxidative Stress and Inflammation

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 July 2023) | Viewed by 956

Special Issue Editors

UNICAEN, CEA, CNRS, ISTCT/CERVOxy Group, GIP CYCERON, Normandie University, 14000 Caen, France
Interests: brain; hypoxia; ischemia; brain tumor; HIFs; imaging; neuroprotection; neuroregeneration
1. Pediatric Onco-Hematology Unit, University Hospital of Strasbourg, 67098 Strasbourg, France
2. UMR CNRS 7021, Laboratory Bioimaging and Pathologies, Tumoral Signaling and Therapeutic Targets, Faculty of Pharmacy, 67401 Illkirch, France
Interests: pediatric high-grade gliomas; advanced Ewing sarcoma or osteosarcoma

Special Issue Information

Dear Colleagues,

The tumor microenvironment (TME) is recognized as an important player and therapeutic target in brain tumors. Each type of tumor has its own TME, and the specificity of the central nervous system is important for taking into account the TME when, for example, regarding the immune response. Different components of the TME in the brain (such as cancer cells, including cancer stem cells, glial cells, neurons, endothelial cells, tumor-infiltrating immune cells, and the extracellular matrix) influence the development and progression of brain tumors and their resistance to anticancer therapies. In addition, among TME features of brain cancers, hypoxia is known to be a poor prognostic factor. It promotes tumor progression through various pathways and induces resistance to cancer treatments including radiotherapy. One of the main cellular responses to hypoxia is the stabilization of the transcription factors, called hypoxia-inducible factors (HIFs). Other factors, such as oxidative stress, determine the formation of a tumor-supportive microenvironment.

This Special Issue, “Brain Tumors and Their Microenvironment: Focus on Hypoxia, Oxidative Stress and Inflammation", aims to give a better characterization of the TME of different aggressive brain tumors, such as glioblastoma and brain metastasis, and its role in tumor growth and treatment response. Therefore, submissions of original research articles or reviews related to the impact of the TME on brain cancer progression and treatment resistance and, in particular, the role of hypoxia, oxidative stress and immunity/inflammation and their interrelationship are encouraged. Various approaches (imaging, transcriptomic, proteomic, etc.) and/or different types of treatment (oxygenation/HIF-related therapies, nanoparticles, different types of radiotherapies, anti- or pro-oxidants, immunotherapies, etc.) will allow us to accumulate the knowledge necessary for the development of new, successful therapeutic approaches for the treatment of brain tumors.

Dr. Myriam Bernaudin
Prof. Dr. Natacha Entz-Werlé
Guest Editors

Manuscript Submission Information

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Keywords

  • brain tumors
  • tumor microenvironment
  • hypoxia/hypoxic signaling
  • oxidative stress/anti- or pro-oxidants
  • metabolism
  • imaging
  • therapeutics
  • inflammation/immunity
  • radioresistance

Published Papers (1 paper)

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Research

20 pages, 4179 KiB  
Article
CXCR2-Blocking Has Context-Sensitive Effects on Rat Glioblastoma Cell Line Outgrowth (S635) in an Organotypic Rat Brain Slice Culture Depending on Microglia-Depletion (PLX5622) and Dexamethasone Treatment
by Johannes Falter, Annette Lohmeier, Petra Eberl, Eva-Maria Stoerr, Janne Koskimäki, Lena Falter, Jakob Rossmann, Tobias Mederer, Nils Ole Schmidt and Martin Proescholdt
Int. J. Mol. Sci. 2023, 24(23), 16803; https://doi.org/10.3390/ijms242316803 - 27 Nov 2023
Viewed by 654
Abstract
In glioblastoma (GBM), the interplay of different immune cell subtypes, cytokines, and/or drugs shows high context-dependencies. Interrelations between the routinely applied dexamethasone (Dex) and microglia remain elusive. Here, we exploited rat organotypic brain slice co-cultures (OBSC) to examine the effects on a rat [...] Read more.
In glioblastoma (GBM), the interplay of different immune cell subtypes, cytokines, and/or drugs shows high context-dependencies. Interrelations between the routinely applied dexamethasone (Dex) and microglia remain elusive. Here, we exploited rat organotypic brain slice co-cultures (OBSC) to examine the effects on a rat GBM cell line (S635) outgrowth resulting from the presence of Dex and pretreatment with the colony-stimulating factor receptor 1 (CSF1-R) inhibitor PLX5622: in native OBSC (without PLX5622-pretreatment), a diminished S635 spheroid outgrowth was observable, whereas Dex-treatment enhanced outgrowth in this condition compared to PLX5622-pretreated OBSC. Screening the supernatants of our model with a proteome profiler, we found that CXCL2 was differentially secreted in a Dex- and PLX5622-dependent fashion. To analyze causal interrelations, we interrupted the CXCL2/CXCR2-axis: in the native OBSC condition, CXCR2-blocking resulted in increased outgrowth, in combination with Dex, we found potentiated outgrowth. No effect was found in the PLX5622-pretreated. Our method allowed us to study the influence of three different factors—dexamethasone, PLX5622, and CXCL2—in a well-controlled, simplified, and straight-forward mechanistic manner, and at the same time in a more realistic ex vivo scenario compared to in vitro studies. In our model, we showed a GBM outgrowth enhancing synergism between CXCR2-blocking and Dex-treatment in the native condition, which was levelled by PLX5622-pretreatment. Full article
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