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Cells
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Molecular and Cellular Mechanisms of Cancers: Glioblastoma III
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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: closed (31 August 2024) | Viewed by 3426

Special Issue Editor

Prof. Dr. Javier S. Castresana

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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

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

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Related Special Issues

Published Papers (4 papers)

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21 pages, 4352 KiB  
Article
PDCD10 Is a Key Player in TMZ-Resistance and Tumor Cell Regrowth: Insights into Its Underlying Mechanism in Glioblastoma Cells
by Yuan Zhu, Su Na Kim, Zhong-Rong Chen, Rainer Will, Rong-De Zhong, Philipp Dammann and Ulrich Sure
Cells 2024, 13(17), 1442; https://doi.org/10.3390/cells13171442 - 28 Aug 2024
Viewed by 345
Abstract
Overcoming temozolomide (TMZ)-resistance is a major challenge in glioblastoma therapy. Therefore, identifying the key molecular player in chemo-resistance becomes urgent. We previously reported the downregulation of PDCD10 in primary glioblastoma patients and its tumor suppressor-like function in glioblastoma cells. Here, we demonstrate that [...] Read more.
Overcoming temozolomide (TMZ)-resistance is a major challenge in glioblastoma therapy. Therefore, identifying the key molecular player in chemo-resistance becomes urgent. We previously reported the downregulation of PDCD10 in primary glioblastoma patients and its tumor suppressor-like function in glioblastoma cells. Here, we demonstrate that the loss of PDCD10 causes a significant TMZ-resistance during treatment and promotes a rapid regrowth of tumor cells after treatment. PDCD10 knockdown upregulated MGMT, a key enzyme mediating chemo-resistance in glioblastoma, accompanied by increased expression of DNA mismatch repair genes, and enabled tumor cells to evade TMZ-induced cell-cycle arrest. These findings were confirmed in independent models of PDCD10 overexpressing cells. Furthermore, PDCD10 downregulation led to the dedifferentiation of glioblastoma cells, as evidenced by increased clonogenic growth, the upregulation of glioblastoma stem cell (GSC) markers, and enhanced neurosphere formation capacity. GSCs derived from PDCD10 knockdown cells displayed stronger TMZ-resistance and regrowth potency, compared to their parental counterparts, indicating that PDCD10-induced stemness may independently contribute to tumor malignancy. These data provide evidence for a dual role of PDCD10 in tumor suppression by controlling both chemo-resistance and dedifferentiation, and highlight PDCD10 as a potential prognostic marker and target for combination therapy with TMZ in glioblastoma. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Glioblastoma III)
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25 pages, 12975 KiB  
Article
3D-Bioprinted Co-Cultures of Glioblastoma Multiforme and Mesenchymal Stromal Cells Indicate a Role for Perivascular Niche Cells in Shaping Glioma Chemokine Microenvironment
by Katarzyna Zielniok, Kinga Rusinek, Anna Słysz, Mieszko Lachota, Ewa Bączyńska, Natalia Wiewiórska-Krata, Anna Szpakowska, Martyna Ciepielak, Bartosz Foroncewicz, Krzysztof Mucha, Radosław Zagożdżon and Zygmunt Pojda
Cells 2024, 13(17), 1404; https://doi.org/10.3390/cells13171404 - 23 Aug 2024
Viewed by 398
Abstract
3D bioprinting has become a valuable tool for studying the biology of solid tumors, including glioblastoma multiforme (GBM). Our analysis of publicly available bulk RNA and single-cell sequencing data has allowed us to define the chemotactic profile of GBM tumors and identify the [...] Read more.
3D bioprinting has become a valuable tool for studying the biology of solid tumors, including glioblastoma multiforme (GBM). Our analysis of publicly available bulk RNA and single-cell sequencing data has allowed us to define the chemotactic profile of GBM tumors and identify the cell types that secrete particular chemokines in the GBM tumor microenvironment (TME). Our findings indicate that primary GBM tissues express multiple chemokines, whereas spherical monocultures of GBM cells significantly lose this diversity. Subsequently, the comparative analysis of GBM spherical monocultures vs. 3D-bioprinted multicultures of cells showed a restoration of chemokine profile diversity in 3D-bioprinted cultures. Furthermore, single-cell RNA-Seq analysis showed that cells of the perivascular niche (pericytes and endocytes) express multiple chemokines in the GBM TME. Next, we 3D-bioprinted cells from two glioblastoma cell lines, U-251 and DK-MG, alone and as co-cultures with mesenchymal stromal cells (representing cells of the perivascular niche) and assessed the chemokine secretome. The results clearly demonstrated that the interaction of tumors and mesenchymal cells leads to in a significant increase in the repertoire and levels of secreted chemokines under culture in 21% O2 and 1% O2. Our study indicates that cells of the perivascular niche may perform a substantial role in shaping the chemokine microenvironment in GBM tumors. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Glioblastoma III)
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16 pages, 3211 KiB  
Article
Evaluation of the Immunomodulatory Effects of Radiation for Chimeric Antigen Receptor T Cell Therapy in Glioblastoma Multiforme
by David Akhavan, Siddharth Subham, John D. Jeppson, Brenda Aguilar, Robyn A. Wong, Jonathan C. Hibbard, Susanta Hui, Jeffrey Y. C. Wong, Stephen J. Forman, Darya Alizadeh and Christine E. Brown
Cells 2024, 13(13), 1075; https://doi.org/10.3390/cells13131075 - 21 Jun 2024
Viewed by 1071
Abstract
Standard-of-care treatment for Glioblastoma Multiforme (GBM) is comprised of surgery and adjuvant chemoradiation. Chimeric Antigen Receptor (CAR) T cell therapy has demonstrated disease-modifying activity in GBM and holds great promise. Radiation, a standard-of-care treatment for GBM, has well-known immunomodulatory properties and may overcome [...] Read more.
Standard-of-care treatment for Glioblastoma Multiforme (GBM) is comprised of surgery and adjuvant chemoradiation. Chimeric Antigen Receptor (CAR) T cell therapy has demonstrated disease-modifying activity in GBM and holds great promise. Radiation, a standard-of-care treatment for GBM, has well-known immunomodulatory properties and may overcome the immunosuppressive tumor microenvironment (TME); however, radiation dose optimization and integration with CAR T cell therapy is not well defined. Murine immunocompetent models of GBM were treated with titrated doses of stereotactic radiosurgery (SRS) of 5, 10, and 20 Gray (Gy), and the TME was analyzed using Nanostring. A conditioning dose of 10 Gy was determined based on tumor growth kinetics and gene expression changes in the TME. We demonstrate that a conditioning dose of 10 Gy activates innate and adaptive immune cells in the TME. Mice treated with 10 Gy in combination with mCAR T cells demonstrated enhanced antitumor activity and superior memory responses to rechallenge with IL13Rα2-positive tumors. Furthermore, 10 Gy plus mCAR T cells also protected against IL13Rα2-negative tumors through a mechanism that was, in part, c-GAS-STING pathway-dependent. Together, these findings support combination conditioning with low-dose 10 Gy radiation in combination with mCAR T cells as a therapeutic strategy for GBM. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Glioblastoma III)
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11 pages, 2251 KiB  
Article
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 1049
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 [...] 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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