Molecular and Cellular Mechanisms of Cancers: Glioblastoma III

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

Deadline for manuscript submissions: 30 June 2024 | Viewed by 879

Special Issue Editor

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Guest Editor
Department of Biochemistry and Genetics, University of Navarra, 31008 Pamplona, Spain
Interests: glioblastoma genetics and epigenetics; brain tumor stem cells; experimental treatments against glioblastoma cells; resistance to therapy
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Special Issue Information

Dear colleagues,

Glioblastoma is the most aggressive brain tumor and one of the tumors with the worst clinical prognosis, with overall survival data of less than two years from diagnosis. Surgically, glioblastoma is difficult to remove due to its infiltrative pattern. This, and the fact that brain tumor stem cells may exist within it, make glioblastoma relapse very frequent. Together with surgery, radiotherapy and chemotherapy are also used for the treatment of this tumor. Temozolomide is the chosen chemotherapy, especially for those patients who do not express MGMT, mostly due to MGMT promoter hypermethylation. However, radiotherapy and temozolomide resistance appear as well. Molecular subtypes of glioblastoma have been established, with the aim of assigning particular therapies to particular tumors.

We invite all scientists working on glioblastoma to contribute to this Special Issue. Original research articles and reviews on all aspects related to the molecular and cellular mechanisms of glioblastoma biology and therapy are welcome. Articles with insights from a cell and molecular biological perspective are especially welcome. Relevant topics include, but are not limited to, the following: genetic and epigenetic profiles, brain tumor stem cells, liquid biopsy, epithelial-to-mesenchymal transition, angiogenesis, migration and invasion, resistance to therapy, molecular and cellular heterogeneity, and any other topics related to the genetics and epigenetics of glioblastoma.

Prof. Dr. Javier S. Castresana
Guest Editor

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  • glioblastoma genetics and epigenetics
  • molecular and cellular heterogeneity of glioblastoma
  • glioblastoma chemoresistance
  • glioblastoma migration, invasion and angiogenesis
  • glioblastoma liquid biopsy
  • glioblastoma targeted therapy
  • brain tumor stem cells
  • epithelial-to-mesenchymal transition in glioblastoma

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Published Papers (1 paper)

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11 pages, 2251 KiB  
The Invasion Factor ODZ1 Is Upregulated through an Epidermal Growth Factor Receptor-Induced Pathway in Primary Glioblastoma Cells
by Carlos Velasquez, Olga Gutierrez, Maria Carcelen and Jose L. Fernandez-Luna
Cells 2024, 13(9), 766; - 30 Apr 2024
Viewed by 582
We have previously shown that the transmembrane protein ODZ1 promotes cytoskeletal remodeling of glioblastoma (GBM) cells and invasion of the surrounding parenchyma through the activation of a RhoA–ROCK pathway. We also described that GBM cells can control the expression of ODZ1 through transcriptional [...] Read more.
We have previously shown that the transmembrane protein ODZ1 promotes cytoskeletal remodeling of glioblastoma (GBM) cells and invasion of the surrounding parenchyma through the activation of a RhoA–ROCK pathway. We also described that GBM cells can control the expression of ODZ1 through transcriptional mechanisms triggered by the binding of IL-6 to its receptor and a hypoxic environment. Epidermal growth factor (EGF) plays a key role in the invasive capacity of GBM. However, the molecular mechanisms that enable tumor cells to acquire the morphological changes to migrate out from the tumor core have not been fully characterized. Here, we show that EGF is able to induce the expression of ODZ1 in primary GBM cells. We analyzed the levels of the EGF receptor (EGFR) in 20 GBM primary cell lines and found expression in 19 of them by flow cytometry. We selected two cell lines that do or do not express the EGFR and found that EGFR-expressing cells responded to the EGF ligand by increasing ODZ1 at the mRNA and protein levels. Moreover, blockade of EGF-EGFR binding by Cetuximab, inhibition of the p38 MAPK pathway, or Additionally, the siRNA-mediated knockdown of MAPK11 (p38β MAPK) reduced the induction of ODZ1 in response to EGF. Overall, we show that EGF may activate an EGFR-mediated signaling pathway through p38β MAPK, to upregulate the invasion factor ODZ1, which may initiate morphological changes for tumor cells to invade the surrounding parenchyma. These data identify a new candidate of the EGF–EGFR pathway for novel therapeutic approaches. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Glioblastoma III)
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