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Cells
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Glioblastoma: What Do We Know?
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Glioblastoma: What Do We Know?

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

Deadline for manuscript submissions: 25 December 2024 | Viewed by 5973

Special Issue Editor

Prof. Dr. Shan Ping Yu

E-Mail Website
Guest Editor
Departments of Anesthesiology, Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA
Interests: cell death mechanisms in brain injuries; degenerative diseases; cancer such as glioblastoma (GBM)

Special Issue Information

Dear Colleagues,

Glioblastoma multiforme (GBM) is a common primary astrocytoma and represents the most malignant tumor in the central nervous system. The fast progression of this tumor and short survival time of GBM patients have been a tough challenge in cancer research and clinical treatment. Despite advances in recent years, GBM remains largely incurable. Little is known about the etiology of GBM, although high-dose ionizing radiation is recognized as a risk factor. GBM shows heterogeneous features involving multiple cell types, including cancer stem cells, hemorrhage, necrosis, aggressive invasion, and vascular endothelial hyperplasia, among other malignant features. Primary and secondary GBMs are characterized by molecular correlates, aberrations of signaling pathways, genetic mutations, and altered gene expression. Early detection and accurate monitoring of carcinoma are critical for early diagnosis, effective treatment, and improved patient outcomes. Biomarkers, such as miRNAs, can be valuable in these applications. In the last few years, genetic modifications, such as the reprogramming of cancer cells into non-cancerous phenotypes, provide an exciting opportunity of stopping tumor growth by a gene therapy. Recent advances in imaging techniques, such as MRI and PET, have also helped in evaluating the changes in the hemodynamics, tissue architecture, and cellular metabolism of gliomas. All of these studies raise the hope for improved therapeutics and the development of a new paradigm for the management of GBM. This Special Issue aims to enhance our knowledge about GBM by sharing the most recent advances in basic and clinical investigations. We welcome articles and reviews of cellular/molecular mechanisms and possible pathogenesis. We especially encourage innovative approaches and strategies that show the potential mechanisms of novel treatments or significantly improved GBM therapy.

Prof. Dr. Shan Ping Yu
Guest Editor

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Keywords

  • carcinoma cell
  • diagnoses
  • molecular mechanism
  • cellular mechanism
  • signaling pathways
  • biomarkers
  • therapeutics

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Published Papers (4 papers)

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Research

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21 pages, 10277 KiB  
Article
Reprogramming Glioblastoma Cells into Non-Cancerous Neuronal Cells as a Novel Anti-Cancer Strategy
by Michael Q. Jiang, Shan Ping Yu, Takira Estaba, Emily Choi, Ken Berglund, Xiaohuan Gu and Ling Wei
Cells 2024, 13(11), 897; https://doi.org/10.3390/cells13110897 - 23 May 2024
Cited by 1 | Viewed by 1601
Abstract
Glioblastoma Multiforme (GBM) is an aggressive brain tumor with a high mortality rate. Direct reprogramming of glial cells to different cell lineages, such as induced neural stem cells (iNSCs) and induced neurons (iNeurons), provides genetic tools to manipulate a cell’s fate as a [...] Read more.
Glioblastoma Multiforme (GBM) is an aggressive brain tumor with a high mortality rate. Direct reprogramming of glial cells to different cell lineages, such as induced neural stem cells (iNSCs) and induced neurons (iNeurons), provides genetic tools to manipulate a cell’s fate as a potential therapy for neurological diseases. NeuroD1 (ND1) is a master transcriptional factor for neurogenesis and it promotes neuronal differentiation. In the present study, we tested the hypothesis that the expression of ND1 in GBM cells can force them to differentiate toward post-mitotic neurons and halt GBM tumor progression. In cultured human GBM cell lines, including LN229, U87, and U373 as temozolomide (TMZ)-sensitive and T98G as TMZ-resistant cells, the neuronal lineage conversion was induced by an adeno-associated virus (AAV) package carrying ND1. Twenty-one days after AAV-ND1 transduction, ND1-expressing cells displayed neuronal markers MAP2, TUJ1, and NeuN. The ND1-induced transdifferentiation was regulated by Wnt signaling and markedly enhanced under a hypoxic condition (2% O2 vs. 21% O2). ND1-expressing GBM cultures had fewer BrdU-positive proliferating cells compared to vector control cultures. Increased cell death was visualized by TUNEL staining, and reduced migrative activity was demonstrated in the wound-healing test after ND1 reprogramming in both TMZ-sensitive and -resistant GBM cells. In a striking contrast to cancer cells, converted cells expressed the anti-tumor gene p53. In an orthotopical GBM mouse model, AAV-ND1-reprogrammed U373 cells were transplanted into the fornix of the cyclosporine-immunocompromised C57BL/6 mouse brain. Compared to control GBM cell-formed tumors, cells from ND1-reprogrammed cultures formed smaller tumors and expressed neuronal markers such as TUJ1 in the brain. Thus, reprogramming using a single-factor ND1 overcame drug resistance, converting malignant cells of heterogeneous GBM cells to normal neuron-like cells in vitro and in vivo. These novel observations warrant further research using patient-derived GBM cells and patient-derived xenograft (PDX) models as a potentially effective treatment for a deadly brain cancer and likely other astrocytoma tumors. Full article
(This article belongs to the Special Issue Glioblastoma: What Do We Know?)
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14 pages, 2784 KiB  
Article
Upregulation of the Renin–Angiotensin System Is Associated with Patient Survival and the Tumour Microenvironment in Glioblastoma
by Mathew Lozinski, Eugenie R. Lumbers, Nikola A. Bowden, Jennifer H. Martin, Michael F. Fay, Kirsty G. Pringle and Paul A. Tooney
Cells 2024, 13(7), 634; https://doi.org/10.3390/cells13070634 - 5 Apr 2024
Viewed by 1310
Abstract
Glioblastoma is a highly aggressive disease with poor survival outcomes. An emerging body of literature links the role of the renin–angiotensin system (RAS), well-known for its function in the cardiovascular system, to the progression of cancers. We studied the expression of RAS-related genes [...] Read more.
Glioblastoma is a highly aggressive disease with poor survival outcomes. An emerging body of literature links the role of the renin–angiotensin system (RAS), well-known for its function in the cardiovascular system, to the progression of cancers. We studied the expression of RAS-related genes (ATP6AP2, AGTR1, AGTR2, ACE, AGT, and REN) in The Cancer Genome Atlas (TCGA) glioblastoma cohort, their relationship to patient survival, and association with tumour microenvironment pathways. The expression of RAS genes was then examined in 12 patient-derived glioblastoma cell lines treated with chemoradiation. In cases of glioblastoma within the TCGA, ATP6AP2, AGTR1, ACE, and AGT had consistent expressions across samples, while AGTR2 and REN were lowly expressed. High expression of AGTR1 was independently associated with lower progression-free survival (PFS) (p = 0.01) and had a non-significant trend for overall survival (OS) after multivariate analysis (p = 0.095). The combined expression of RAS receptors (ATP6AP2, AGTR1, and AGTR2) was positively associated with gene pathways involved in hypoxia, microvasculature, stem cell plasticity, and the molecular characterisation of glioblastoma subtypes. In patient-derived glioblastoma cell lines, ATP6AP2 and AGTR1 were upregulated after chemoradiotherapy and correlated with an increase in HIF1A expression. This data suggests the RAS is correlated with changes in the tumour microenvironment and associated with glioblastoma survival outcomes. Full article
(This article belongs to the Special Issue Glioblastoma: What Do We Know?)
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14 pages, 2852 KiB  
Article
CD99 Expression and Prognostic Impact in Glioblastoma: A Single-Center Cohort Study
by Andrea Rocca, Fabiola Giudici, Carmine Antonio Donofrio, Cristina Bottin, Maurizio Pinamonti, Benvenuto Ferrari, Francesco Schettini, Estela Pineda, Stefano Panni, Marika Cominetti, Patrizia D’Auria, Simonetta Bianchini, Elena Varotti, Marco Ungari, Stefano Ciccarelli, Marzia Filippini, Sarah Brenna, Valentina Fiori, Tomas Di Mambro, Angelo Sparti, Mauro Magnani, Fabrizio Zanconati, Daniele Generali and Antonio Fioravantiadd Show full author list remove Hide full author list
Cells 2024, 13(7), 597; https://doi.org/10.3390/cells13070597 - 29 Mar 2024
Viewed by 1486
Abstract
Glioblastoma is the most frequent and aggressive brain tumor in adults. This study aims to evaluate the expression and prognostic impact of CD99, a membrane glycoprotein involved in cellular migration and invasion. In a cohort of patients with glioblastoma treated with surgery, radiotherapy [...] Read more.
Glioblastoma is the most frequent and aggressive brain tumor in adults. This study aims to evaluate the expression and prognostic impact of CD99, a membrane glycoprotein involved in cellular migration and invasion. In a cohort of patients with glioblastoma treated with surgery, radiotherapy and temozolomide, we retrospectively analyzed tumor expression of CD99 by immunohistochemistry (IHC) and by quantitative real-time polymerase chain reaction (qRT-PCR) for both the wild type (CD99wt) and the truncated (CD99sh) isoforms. The impact on overall survival (OS) was assessed with the Kaplan–Meier method and log-rank test and by multivariable Cox regression. Forty-six patients with glioblastoma entered this study. Immunohistochemical expression of CD99 was present in 83%. Only the CD99wt isoform was detected by qRT-PCR and was significantly correlated with CD99 expression evaluated by IHC (rho = 0.309, p = 0.037). CD99 expression was not associated with OS, regardless of the assessment methodology used (p = 0.61 for qRT-PCR and p = 0.73 for IHC). In an exploratory analysis of The Cancer Genome Atlas, casuistry of glioblastomas CD99 expression was not associated with OS nor with progression-free survival. This study confirms a high expression of CD99 in glioblastoma but does not show any significant impact on survival. Further preclinical studies are needed to define its role as a therapeutic target in glioblastoma. Full article
(This article belongs to the Special Issue Glioblastoma: What Do We Know?)
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Review

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30 pages, 2044 KiB  
Review
Metabolic Reprogramming in Glioblastoma Multiforme: A Review of Pathways and Therapeutic Targets
by Ashley Irin Cortes Ballen, Maryam Amosu, Surya Ravinder, Joey Chan, Emre Derin, Hasan Slika and Betty Tyler
Cells 2024, 13(18), 1574; https://doi.org/10.3390/cells13181574 - 19 Sep 2024
Viewed by 976
Abstract
Glioblastoma (GBM) is an aggressive and highly malignant primary brain tumor characterized by rapid growth and a poor prognosis for patients. Despite advancements in treatment, the median survival time for GBM patients remains low. One of the crucial challenges in understanding and treating [...] Read more.
Glioblastoma (GBM) is an aggressive and highly malignant primary brain tumor characterized by rapid growth and a poor prognosis for patients. Despite advancements in treatment, the median survival time for GBM patients remains low. One of the crucial challenges in understanding and treating GBMs involves its remarkable cellular heterogeneity and adaptability. Central to the survival and proliferation of GBM cells is their ability to undergo metabolic reprogramming. Metabolic reprogramming is a process that allows cancer cells to alter their metabolism to meet the increased demands of rapid growth and to survive in the often oxygen- and nutrient-deficient tumor microenvironment. These changes in metabolism include the Warburg effect, alterations in several key metabolic pathways including glutamine metabolism, fatty acid synthesis, and the tricarboxylic acid (TCA) cycle, increased uptake and utilization of glutamine, and more. Despite the complexity and adaptability of GBM metabolism, a deeper understanding of its metabolic reprogramming offers hope for developing more effective therapeutic interventions against GBMs. Full article
(This article belongs to the Special Issue Glioblastoma: What Do We Know?)
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