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Glioblastoma Microenvironment and Cellular Interactions

Crivii, Carmen-Bianca, Boșca, Adina Bianca, Melincovici, Carmen Stanca, Constantin, Anne-Marie, Mărginean, Mariana, Dronca, Eleonora, Suflețel, Rada, Gonciar, Diana, Bungărdean, Maria, Șovrea, Alina·2022·Cancers
DOI 10.3390/cancers14041092PMC PMC8870579
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Abstract

The central nervous system (CNS) represents a complex network of different cells, such as neurons, glial cells, and blood vessels. In tumor pathology, glial cells result in the highest number of cancers, and glioblastoma (GB) is considered the most lethal tumor in this region. The development of GB leads to the infiltration of healthy tissue through the interaction between all the elements of the brain network. This results in a GB microenvironment, a complex peritumoral hallo composed of tumor cells and several non-tumor cells (e.g., nervous cells, stem cells, fibroblasts, vascular and immune cells), which might be the principal factor for the ineffective treatment due to the fact that the microenvironment modulates the biologic status of the tumor with the increase in its evasion capacity. Crosstalk between glioma cells and the brain microenvironment finally inhibits the beneficial action of molecular pathways, favoring the development and invasion of the tumor and its increasing resistance to treatment. A deeper understanding of cell–cell interactions in the tumor microenvironment (TME) and with the tumor cells could be the basis for a more efficient therapy.

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Figure 1 Intercellular communication between GBM and TME—direct exchange via EVs. EVs transport different cargo between GBM cells and TME, passing through the BBB by disrupting it. This is due to Semaphorin3A present on their surface that binds to its receptor on the BBB, the neuropilin1.
Figure 1 Intercellular communication between GBM and TME—direct exchange via EVs. EVs transport different cargo between GBM cells and TME, passing through the BBB by disrupting it. This is due to Semaphorin3A present on their surface that binds to its receptor on the BBB, the neuropilin1.CC BY · PubMed Central
Figure 2 Intercellular communication between GBM and TME—direct exchange via GJs between glioma cells and astrocytes. When CX-43 increases, it leads to GBM cell proliferation and migration, overall enhancing chemotherapy resistance.
Figure 2 Intercellular communication between GBM and TME—direct exchange via GJs between glioma cells and astrocytes. When CX-43 increases, it leads to GBM cell proliferation and migration, overall enhancing chemotherapy resistance.CC BY · PubMed Central
Figure 3 Intercellular communication between GBM and TME—direct exchange via ion channels (it is leading to cell volume and shape variations or loss of epithelial polarization by ion concentration changes).
Figure 3 Intercellular communication between GBM and TME—direct exchange via ion channels (it is leading to cell volume and shape variations or loss of epithelial polarization by ion concentration changes).CC BY · PubMed Central
Figure 4 Epithelial to mesenchymal transition of GBM cells passing through an intermediate phase where both epithelial and mesenchymal features are present. Note that this process is reversible, and it implies acquisition and loss of markers.
Figure 4 Epithelial to mesenchymal transition of GBM cells passing through an intermediate phase where both epithelial and mesenchymal features are present. Note that this process is reversible, and it implies acquisition and loss of markers.CC BY · PubMed Central
Figure 5 Pathogenic mechanisms underlying the role of reactive astrocytes in GB development and progression. Astrocytes can undergo malignant transformation to promote gliomagenesis, but can also become activated, as components with essential influence on the TME. Tumor-associated reactive astrocytes exhibit morphological, functional, and metabolic changes and, by their interaction with glioma cells, can either suppress or promote tumor maintenance and invasion, as well as resistance to chemo-radiotherapy.
Figure 5 Pathogenic mechanisms underlying the role of reactive astrocytes in GB development and progression. Astrocytes can undergo malignant transformation to promote gliomagenesis, but can also become activated, as components with essential influence on the TME. Tumor-associated reactive astrocytes exhibit morphological, functional, and metabolic changes and, by their interaction with glioma cells, can either suppress or promote tumor maintenance and invasion, as well as resistance to chemo-radiotherapy.CC BY · PubMed Central
Figure 6 GBM cells secrete chemoattractant factors through which they recruit TAM. By the two polarization states, M1 and M2, TAM may trigger regression or progression of GBM.
Figure 6 GBM cells secrete chemoattractant factors through which they recruit TAM. By the two polarization states, M1 and M2, TAM may trigger regression or progression of GBM.CC BY · PubMed Central

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Metadata

Authors
Crivii, C.-B., Boșca, A. B., Melincovici, C. S., Constantin, A.-M., Mărginean, M., Dronca, E., Suflețel, R., Gonciar, D., Bungărdean, M., & Șovrea, A.
Affiliations
  • Anatomy and Embryology Discipline, Morphological Sciences Department, Iuliu Hațieganu University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania
  • Histology Discipline, Morphological Sciences Department, Iuliu Hațieganu University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania
  • Medical Genetics Discipline, Molecular Sciences Department, Iuliu Hațieganu University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania
  • Pathological Anatomy Discipline, Morphological Sciences Department, Iuliu Hațieganu University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania
ORCID
Crivii, Carmen-Bianca
Venue
Cancers
Publisher
MDPI AG
Published
2022-02-21
Volume
14
Issue
4
Pages
1092
ISSN
2072-6694
DOI
10.3390/cancers14041092
PMC
PMC8870579
Cited by
81
References
17
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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