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Special Issue "Glioblastoma – Pathogenesis, Cellular and Molecular Mechanism"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2020).

Special Issue Editor

Dr. Maurizio Martini
E-Mail Website
Guest Editor
Institute of Pathology, Catholic University of Sacred Heart, Largo A. Gemelli 8, 00168, Rome, Italy
Interests: hematopathology; glial and central nervous system cancer; gastrointestinal tumor; lung cancer; thyroid cancer; genitourinary cancer

Special Issue Information

Dear Colleagues,

Glioblastoma (GBM) is the most frequent and aggressive primary adult brain tumor with about 5% survival rate at 5 years. Even with the current multimodal therapy, including targeted and anti-angiogenetic therapy, the mean survival of GBM patients is still approximately 15 months. Because of its extremely unfavorable prognosis, it is imperative to investigate new possible altered molecular mechanisms involved in the GBM pathogenesis that can translate in the development of a more effective therapeutic strategies for this cancer. This Special Issue of the International Journal of Molecular Sciences, entitled “Glioblastoma – Pathogenesis, Cellular and Molecular Mechanism” will focus on how intracellular molecular pathways are altered in tumor cells. Authors are invited to submit manuscripts that analyze molecular mechanisms possibly involved in GBM pathogenesis, such as cancer stem cells, apoptosis and autophagia, kinome, cell cycle and metabolism, angiogenesis, lncRNA, miRNA and RNA editing pathways. The results from these studies may provide useful information in devising treatments that may enhance survival rates of GBM patients.

Dr. Maurizio Martini
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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • Cancer stem cells
  • Kinase pathways
  • Angiogenesis
  • Oncogenes
  • Tumor suppressor genes
  • lnRNA, miRNA
  • RNA editing mechanism

Published Papers (4 papers)

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Open AccessArticle
DNA Methylation Analysis Identifies Patterns in Progressive Glioma Grades to Predict Patient Survival
Int. J. Mol. Sci. 2021, 22(3), 1020; https://doi.org/10.3390/ijms22031020 - 20 Jan 2021
Cited by 1 | Viewed by 638 | Correction
Abstract
DNA methylation is an epigenetic change to the genome that impacts gene activities without modification to the DNA sequence. Alteration in the methylation pattern is a naturally occurring event throughout the human life cycle which may result in the development of diseases such [...] Read more.
DNA methylation is an epigenetic change to the genome that impacts gene activities without modification to the DNA sequence. Alteration in the methylation pattern is a naturally occurring event throughout the human life cycle which may result in the development of diseases such as cancer. In this study, we analyzed methylation data from The Cancer Genome Atlas, under the Lower-Grade Glioma (LGG) and Glioblastoma Multiforme (GBM) projects, to identify methylation markers that exhibit unique changes in DNA methylation pattern along with tumor grade progression, to predict patient survival. We found ten glioma grade-associated Cytosine-phosphate-Guanine (CpG) sites that targeted four genes (SMOC1, KCNA4, SLC25A21, and UPP1) and the methylation pattern is strongly associated with glioma specific molecular alterations, primarily isocitrate dehydrogenase (IDH) mutation and chromosome 1p/19q codeletion. The ten CpG sites collectively distinguished a cohort of diffuse glioma patients with remarkably poor survival probability. Our study highlights genes (KCNA4 and SLC25A21) that were not previously associated with gliomas to have contributed to the poorer patient outcome. These CpG sites can aid glioma tumor progression monitoring and serve as prognostic markers to identify patients diagnosed with less aggressive and malignant gliomas that exhibit similar survival probability to GBM patients. Full article
(This article belongs to the Special Issue Glioblastoma – Pathogenesis, Cellular and Molecular Mechanism)
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Open AccessArticle
CKAP2L Knockdown Exerts Antitumor Effects by Increasing miR-4496 in Glioblastoma Cell Lines
Int. J. Mol. Sci. 2021, 22(1), 197; https://doi.org/10.3390/ijms22010197 - 27 Dec 2020
Viewed by 706
Abstract
Despite advances in the diagnosis and treatment of the central nervous system malignancy glioma, overall survival remains poor. Cytoskeleton-associated protein 2-like (CKAP2L), which plays key roles in neural progenitor cell division, has also been linked to poor prognosis in lung cancer. [...] Read more.
Despite advances in the diagnosis and treatment of the central nervous system malignancy glioma, overall survival remains poor. Cytoskeleton-associated protein 2-like (CKAP2L), which plays key roles in neural progenitor cell division, has also been linked to poor prognosis in lung cancer. In the present study, we investigated the role of CKAP2L in glioma. From bioinformatics analyses of datasets from The Cancer Gene Atlas and the Chinese Glioma Genome Atlas, we found that CKAP2L expression correlates with tumor grade and overall survival. Gene set enrichment analysis (GSEA) showed that MITOTIC_SPINDLE, G2M_CHECKPOINT, and E2F_TARGETS are crucially enriched phenotypes associated with high CKAP2L expression. Using U87MG, U118MG, and LNZ308 human glioma cells, we confirmed that CKAP2L knockdown with siCKAP2L inhibits glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition. Interestingly, CKAP2L knockdown also induced cell cycle arrest at G2/M phase, which is consistent with the GSEA finding. Finally, we observed that CKAP2L knockdown led to significant increases in miR-4496. Treating cells with exogenous miR-4496 mimicked the effect of CKAP2L knockdown, and the effects of CKAP2L knockdown could be suppressed by miR-4496 inhibition. These findings suggest that CKAP2L is a vital regulator of miR-4496 activity and that CKAP2L is a potentially useful prognostic marker in glioma. Full article
(This article belongs to the Special Issue Glioblastoma – Pathogenesis, Cellular and Molecular Mechanism)
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Open AccessArticle
High Adenosine Extracellular Levels Induce Glioblastoma Aggressive Traits Modulating the Mesenchymal Stromal Cell Secretome
Int. J. Mol. Sci. 2020, 21(20), 7706; https://doi.org/10.3390/ijms21207706 - 18 Oct 2020
Cited by 2 | Viewed by 515
Abstract
Glioblastoma is an aggressive, fast-growing brain tumor influenced by the composition of the tumor microenvironment (TME) in which mesenchymal stromal cell (MSCs) play a pivotal role. Adenosine (ADO), a purinergic signal molecule, can reach up to high micromolar concentrations in TME. The activity [...] Read more.
Glioblastoma is an aggressive, fast-growing brain tumor influenced by the composition of the tumor microenvironment (TME) in which mesenchymal stromal cell (MSCs) play a pivotal role. Adenosine (ADO), a purinergic signal molecule, can reach up to high micromolar concentrations in TME. The activity of specific adenosine receptor subtypes on glioma cells has been widely explored, as have the effects of MSCs on tumor progression. However, the effects of high levels of ADO on glioma aggressive traits are still unclear as is its role in cancer cells-MSC cross-talk. Herein, we first studied the role of extracellular Adenosine (ADO) on isolated human U343MG cells as a glioblastoma cellular model, finding that at high concentrations it was able to prompt the gene expression of Snail and ZEB1, which regulate the epithelial–mesenchymal transition (EMT) process, even if a complete transition was not reached. These effects were mediated by the induction of ERK1/2 phosphorylation. Additionally, ADO affected isolated bone marrow derived MSCs (BM-MSCs) by modifying the pattern of secreted inflammatory cytokines. Then, the conditioned medium (CM) of BM-MSCs stimulated with ADO and a co-culture system were used to investigate the role of extracellular ADO in GBM–MSC cross-talk. The CM promoted the increase of glioma motility and induced a partial phenotypic change of glioblastoma cells. These effects were maintained when U343MG cells and BM-MSCs were co-cultured. In conclusion, ADO may affect glioma biology directly and through the modulation of the paracrine factors released by MSCs overall promoting a more aggressive phenotype. These results point out the importance to deeply investigate the role of extracellular soluble factors in the glioma cross-talk with other cell types of the TME to better understand its pathological mechanisms. Full article
(This article belongs to the Special Issue Glioblastoma – Pathogenesis, Cellular and Molecular Mechanism)
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Open AccessCorrection
Correction: Weng, J., et al. DNA Methylation Analysis Identifies Patterns in Progressive Glioma Grades to Predict Patient Survival. Int. J. Mol. Sci. 2021, 22, 1020
Int. J. Mol. Sci. 2021, 22(8), 3842; https://doi.org/10.3390/ijms22083842 - 08 Apr 2021
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Abstract
The authors wish to make the following corrections to paper “DNA Methylation Analysis Identifies Patterns in Progressive Glioma Grades to Predict Patient Survival” [...] Full article
(This article belongs to the Special Issue Glioblastoma – Pathogenesis, Cellular and Molecular Mechanism)
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