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Cancers
Special Issues
Oncogenes and Tumor Suppressor Genes in Brain Tumor
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Oncogenes and Tumor Suppressor Genes in Brain Tumor

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 13147

Special Issue Editor

Prof. Dr. Mojgan Rastegar

E-Mail Website
Guest Editor
Department of Biochemistry and Medical Genetics, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada
Interests: epigenetics; DNA methylation; transcriptional control; gene regulation; drug repurposing; neural stem cells; neurodevelopmental disorders; medulloblastoma brain tumor
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain tumors are associated with abnormal growth of cellular mass in different brain regions. A hallmark of cancer cells is deregulation of cellular proliferation, differentiation, and survival. This is frequently associated with altered expression of oncogenes and tumor suppressor genes in cancer cells as they keep the cellular balance between the normal and cancerous cellular states. Oncogenes are specific proteins that are capable of inducing cell-transformation-causing cancer. Generally, gain-of-function mutation of proto-oncogenes would lead to increased cellular growth, proliferation, and cancer. On the other hand, loss-of-function mutations in tumor suppressor genes lead to deregulated cellular division, which is associated with different types of cancer.

Induction of oncogenes and absence of tumor suppressor genes would trigger certain cellular pathways that control cell cycle, cell survival, cell growth, with a direct link to tumorigenicity depending on the context. Developing an understanding about how different cell types regulate the expression of oncogenes and tumor suppressor genes is of important significance. However, despite intensive research, we are still not fully clear on how to manage the downstream signaling pathways and upstream regulatory mechanism in order for the best clinical outcome.

This Special Issue will cover downstream signaling pathways for oncogenes and tumor suppressor genes, their upstream regulators, their control mechanisms (at the level of epigenetics, transcription, translation, protein homeostasis), and the outcome of their mutation affecting cellular survival, differentiation, and proliferation. While different primary or metastatic brain tumors will be considered, manuscripts focusing on medulloblastomas and gliomas are encouraged. In addition, manuscripts linking oncogenes and tumor suppressor genes to regulatory cellular mechanisms, such as proteosome pathway, cellular metabolism, and cell death machinery (including autophagy, apoptosis), are welcome for submission.

Prof. Dr. Mojgan Rastegar
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. Cancers 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 2900 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

  • brain tumor
  • medulloblastoma
  • glioblastoma
  • oncogenes
  • tumor suppressor genes
  • P53
  • proteosome pathway
  • cellular metabolism
  • cell death machinery
  • autophagy
  • apoptosis

Published Papers (5 papers)

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Research

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13 pages, 6319 KiB  
Article
BRMS1 in Gliomas—An Expression Analysis
by Jonas Feldheim, Almuth F. Kessler, Julia J. Feldheim, Dominik Schmitt, Christoph Oster, Lazaros Lazaridis, Martin Glas, Ralf-Ingo Ernestus, Camelia M. Monoranu, Mario Löhr and Carsten Hagemann
Cancers 2023, 15(11), 2907; https://doi.org/10.3390/cancers15112907 - 25 May 2023
Viewed by 942
Abstract
The metastatic suppressor BRMS1 interacts with critical steps of the metastatic cascade in many cancer entities. As gliomas rarely metastasize, BRMS1 has mainly been neglected in glioma research. However, its interaction partners, such as NFκB, VEGF, or MMPs, are old acquaintances in neurooncology. [...] Read more.
The metastatic suppressor BRMS1 interacts with critical steps of the metastatic cascade in many cancer entities. As gliomas rarely metastasize, BRMS1 has mainly been neglected in glioma research. However, its interaction partners, such as NFκB, VEGF, or MMPs, are old acquaintances in neurooncology. The steps regulated by BRMS1, such as invasion, migration, and apoptosis, are commonly dysregulated in gliomas. Therefore, BRMS1 shows potential as a regulator of glioma behavior. By bioinformatic analysis, in addition to our cohort of 118 specimens, we determined BRMS1 mRNA and protein expression as well as its correlation with the clinical course in astrocytomas IDH mutant, CNS WHO grade 2/3, and glioblastoma IDH wild-type, CNS WHO grade 4. Interestingly, we found BRMS1 protein expression to be significantly decreased in the aforementioned gliomas, while BRMS1 mRNA appeared to be overexpressed throughout. This dysregulation was independent of patients’ characteristics or survival. The protein and mRNA expression differences cannot be finally explained at this stage. However, they suggest a post-transcriptional dysregulation that has been previously described in other cancer entities. Our analyses present the first data on BRMS1 expression in gliomas that can provide a starting point for further investigations. Full article
(This article belongs to the Special Issue Oncogenes and Tumor Suppressor Genes in Brain Tumor)
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15 pages, 2173 KiB  
Article
Genetic Alterations and Resectability Predict Outcome in Patients with Neuroblastoma Assigned to High-Risk Solely by MYCN Amplification
by Frank Berthold, Angela Ernst, Sandra Ackermann, Christoph Bartenhagen, Holger Christiansen, Barbara Hero, Carolina Rosswog, Dietrich von Schweinitz, Thomas Klingebiel, Irene Schmid, Thorsten Simon and Matthias Fischer
Cancers 2021, 13(17), 4360; https://doi.org/10.3390/cancers13174360 - 28 Aug 2021
Cited by 1 | Viewed by 1731
Abstract
Background: To identify variables predicting outcome in neuroblastoma patients assigned to the high-risk group solely by the presence of MYCN oncogene amplification (MNA). Methods: Clinical characteristics, genomic information, and outcome of 190 patients solely assigned to high-risk neuroblastoma by MNA were analyzed and [...] Read more.
Background: To identify variables predicting outcome in neuroblastoma patients assigned to the high-risk group solely by the presence of MYCN oncogene amplification (MNA). Methods: Clinical characteristics, genomic information, and outcome of 190 patients solely assigned to high-risk neuroblastoma by MNA were analyzed and compared to 205 patients with stage 4 neuroblastoma aged ≥18 months with MNA (control group). Results: Event-free survival (EFS) and overall survival (OS) at 10 years were 47% (95%-CI 39–54%) and 56% (95%-CI 49–63%), respectively, which was significantly better than EFS and OS of the control group (EFS 25%, 95%-CI 18–31%, p < 0.001; OS 32% 95%-CI 25–39%, p < 0.001). The presence of RAS-/p53-pathway gene alterations was associated with impaired 10-year EFS and OS (19% vs. 55%, and 19% vs. 67%, respectively; both p < 0.001). In time-dependent multivariable analyses, alterations of RAS-/p53-pathway genes and the extent of the best primary tumor resection were the only independent prognostic variables for OS (p < 0.001 and p = 0.011, respectively). Conclusions: Neuroblastoma patients attributed to high risk solely by MYCN amplification have generally a more favorable outcome. Mutations of genes of the RAS and/or p53 pathways and incomplete resection are the main risk factors predicting poor outcome. Full article
(This article belongs to the Special Issue Oncogenes and Tumor Suppressor Genes in Brain Tumor)
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Review

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22 pages, 3380 KiB  
Review
The Epigenetic Reader Methyl-CpG-Binding Protein 2 (MeCP2) Is an Emerging Oncogene in Cancer Biology
by Kazem Nejati-Koshki, Chris-Tiann Roberts, Ghader Babaei and Mojgan Rastegar
Cancers 2023, 15(10), 2683; https://doi.org/10.3390/cancers15102683 - 09 May 2023
Cited by 6 | Viewed by 2298
Abstract
Epigenetic mechanisms are gene regulatory processes that control gene expression and cellular identity. Epigenetic factors include the “writers”, “readers”, and “erasers” of epigenetic modifications such as DNA methylation. Accordingly, the nuclear protein Methyl-CpG-Binding Protein 2 (MeCP2) is a reader of DNA methylation with [...] Read more.
Epigenetic mechanisms are gene regulatory processes that control gene expression and cellular identity. Epigenetic factors include the “writers”, “readers”, and “erasers” of epigenetic modifications such as DNA methylation. Accordingly, the nuclear protein Methyl-CpG-Binding Protein 2 (MeCP2) is a reader of DNA methylation with key roles in cellular identity and function. Research studies have linked altered DNA methylation, deregulation of MeCP2 levels, or MECP2 gene mutations to different types of human disease. Due to the high expression level of MeCP2 in the brain, many studies have focused on its role in neurological and neurodevelopmental disorders. However, it is becoming increasingly apparent that MeCP2 also participates in the tumorigenesis of different types of human cancer, with potential oncogenic properties. It is well documented that aberrant epigenetic regulation such as altered DNA methylation may lead to cancer and the process of tumorigenesis. However, direct involvement of MeCP2 with that of human cancer was not fully investigated until lately. In recent years, a multitude of research studies from independent groups have explored the molecular mechanisms involving MeCP2 in a vast array of human cancers that focus on the oncogenic characteristics of MeCP2. Here, we provide an overview of the proposed role of MeCP2 as an emerging oncogene in different types of human cancer. Full article
(This article belongs to the Special Issue Oncogenes and Tumor Suppressor Genes in Brain Tumor)
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56 pages, 3598 KiB  
Review
Synthesis and Significance of Arachidonic Acid, a Substrate for Cyclooxygenases, Lipoxygenases, and Cytochrome P450 Pathways in the Tumorigenesis of Glioblastoma Multiforme, Including a Pan-Cancer Comparative Analysis
by Jan Korbecki, Ewa Rębacz-Maron, Patrycja Kupnicka, Dariusz Chlubek and Irena Baranowska-Bosiacka
Cancers 2023, 15(3), 946; https://doi.org/10.3390/cancers15030946 - 02 Feb 2023
Cited by 7 | Viewed by 4138
Abstract
Glioblastoma multiforme (GBM) is one of the most aggressive gliomas. New and more effective therapeutic approaches are being sought based on studies of the various mechanisms of GBM tumorigenesis, including the synthesis and metabolism of arachidonic acid (ARA), an omega-6 polyunsaturated fatty acid [...] Read more.
Glioblastoma multiforme (GBM) is one of the most aggressive gliomas. New and more effective therapeutic approaches are being sought based on studies of the various mechanisms of GBM tumorigenesis, including the synthesis and metabolism of arachidonic acid (ARA), an omega-6 polyunsaturated fatty acid (PUFA). PubMed, GEPIA, and the transcriptomics analysis carried out by Seifert et al. were used in writing this paper. In this paper, we discuss in detail the biosynthesis of this acid in GBM tumors, with a special focus on certain enzymes: fatty acid desaturase (FADS)1, FADS2, and elongation of long-chain fatty acids family member 5 (ELOVL5). We also discuss ARA metabolism, particularly its release from cell membrane phospholipids by phospholipase A2 (cPLA2, iPLA2, and sPLA2) and its processing by cyclooxygenases (COX-1 and COX-2), lipoxygenases (5-LOX, 12-LOX, 15-LOX-1, and 15-LOX-2), and cytochrome P450. Next, we discuss the significance of lipid mediators synthesized from ARA in GBM cancer processes, including prostaglandins (PGE2, PGD2, and 15-deoxy-Δ12,14-PGJ2 (15d-PGJ2)), thromboxane A2 (TxA2), oxo-eicosatetraenoic acids, leukotrienes (LTB4, LTC4, LTD4, and LTE4), lipoxins, and many others. These lipid mediators can increase the proliferation of GBM cancer cells, cause angiogenesis, inhibit the anti-tumor response of the immune system, and be responsible for resistance to treatment. Full article
(This article belongs to the Special Issue Oncogenes and Tumor Suppressor Genes in Brain Tumor)
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23 pages, 1424 KiB  
Review
The Role of microRNAs in Multidrug Resistance of Glioblastoma
by Parvaneh Mahinfar, Behnaz Mansoori, Davoud Rostamzadeh, Behzad Baradaran, William C. Cho and Behzad Mansoori
Cancers 2022, 14(13), 3217; https://doi.org/10.3390/cancers14133217 - 30 Jun 2022
Cited by 9 | Viewed by 2557
Abstract
Glioblastoma (GBM) is an aggressive brain tumor that develops from neuroglial stem cells and represents a highly heterogeneous group of neoplasms. These tumors are predominantly correlated with a dismal prognosis and poor quality of life. In spite of major advances in developing novel [...] Read more.
Glioblastoma (GBM) is an aggressive brain tumor that develops from neuroglial stem cells and represents a highly heterogeneous group of neoplasms. These tumors are predominantly correlated with a dismal prognosis and poor quality of life. In spite of major advances in developing novel and effective therapeutic strategies for patients with glioblastoma, multidrug resistance (MDR) is considered to be the major reason for treatment failure. Several mechanisms contribute to MDR in GBM, including upregulation of MDR transporters, alterations in the metabolism of drugs, dysregulation of apoptosis, defects in DNA repair, cancer stem cells, and epithelial–mesenchymal transition. MicroRNAs (miRNAs) are a large class of endogenous RNAs that participate in various cell events, including the mechanisms causing MDR in glioblastoma. In this review, we discuss the role of miRNAs in the regulation of the underlying mechanisms in MDR glioblastoma which will open up new avenues of inquiry for the treatment of glioblastoma. Full article
(This article belongs to the Special Issue Oncogenes and Tumor Suppressor Genes in Brain Tumor)
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