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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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

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

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

Related Special Issues

Published Papers (1 paper)

Research

11 pages, 2251 KiB

Open AccessArticle

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; https://doi.org/10.3390/cells13090766 - 30 Apr 2024

Viewed by 356

Abstract

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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