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Cells
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Molecular Mechanisms and Therapeutic Interventions of Glioma
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Molecular Mechanisms and Therapeutic Interventions of Glioma

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

Deadline for manuscript submissions: closed (10 July 2023) | Viewed by 5850

Special Issue Editor

Dr. Kai Zheng

E-Mail Website
Guest Editor
Health Science Center, School of Pharmaceutical Sciences, Shenzhen University, Shenzhen 518060, China
Interests: autophagy; cancer therapy; DNA damage; cellular senescence; bioinformatics; molecular microbiology; antiviral and anticancer pharmacology; metabolites

Special Issue Information

Dear Colleagues,

Glioma is the most severe and fatal form of brain cancer in adults and is generally classified as primary and secondary with several different subtypes. Although growing understanding of the various mechanisms of intra- and intertumoral heterogeneity, immunosuppressive microenvironment, and acquired resistance to the conventional induction of apoptosis, clinical trials in the field are still largely disappointing. Genetic alterations (e.g., EGFR, IDH, PTEN, p53, HIF) and extrinsic environmental factors (e.g., cytokines, proteins, extracellular vesicles) have been confirmed to promote tumor surveillance and disease progression. Moreover, there is increasing evidence that multi-organ crosstalk, such as microbiota–gut–brain axis, affects the molecular biological properties of gliomas. Clarifying these complex mechanisms are inevitably necessary to identify novel therapeutic targets and strategies. Alternatively, the emergency of other non-canonical lysosome-dependent or independent cell death mechanisms (Cuprotosis, Ferroptosis, Necroptosis, Pyroptosis, and Anoikis) encourages the discovering new therapeutic opportunities, beyond the conventional therapies (e.g., chemotherapy, radiotherapy, targeted therapy) in glioma, which may overcome the tumor cell heterogeneity and adverse immunosuppressive microenvironment. Furthermore, organoids are important platforms for discovering the diagnosis biomarker, potential therapeutic treatments, progressive physiological characteristics and molecular mechanisms of glioma.

In this Special Issue entitled “Molecular Mechanisms and Therapeutic Interventions of Glioma”, we invite you to contribute with original research articles, reviews, multi-omics analysis (with experimental consolidation) or short perspective articles on all aspects related with molecular mechanisms, diagnostic and prognostic biomarkers, preclinical models and therapeutic options of glioma.

Dr. Kai Zheng
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

  • glioma
  • cell death mechanism
  • signaling pathways
  • metabolism
  • organoids
  • microbiota-gut-brain axis
  • pharmaceutics
  • immunotherapy
  • heterogeneity
  • biomarkers

Published Papers (3 papers)

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Research

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12 pages, 3445 KiB  
Communication
Enhanced Sensitivity to ALDH1A3-Dependent Ferroptosis in TMZ-Resistant Glioblastoma Cells
by Yang Wu, Sophie Franzmeier, Friederike Liesche-Starnecker and Jürgen Schlegel
Cells 2023, 12(21), 2522; https://doi.org/10.3390/cells12212522 - 25 Oct 2023
Cited by 3 | Viewed by 1521
Abstract
Temozolomide (TMZ) is standard treatment for glioblastoma (GBM); nonetheless, resistance and tumor recurrence are still major problems. In addition to its association with recurrent GBM and TMZ resistance, ALDH1A3 has a role in autophagy-dependent ferroptosis activation. In this study, we treated TMZ-resistant LN229 [...] Read more.
Temozolomide (TMZ) is standard treatment for glioblastoma (GBM); nonetheless, resistance and tumor recurrence are still major problems. In addition to its association with recurrent GBM and TMZ resistance, ALDH1A3 has a role in autophagy-dependent ferroptosis activation. In this study, we treated TMZ-resistant LN229 human GBM cells with the ferroptosis inducer RSL3. Remarkably, TMZ-resistant LN229 clones were also resistant to ferroptosis induction, although lipid peroxidation was induced by RSL3. By using Western blotting, we were able to determine that ALDH1A3 was down-regulated in TMZ-resistant LN229 cells. Most intriguingly, the cell viability results showed that only those clones that up-regulated ALDH1A3 after TMZ withdrawal became re-sensitized to ferroptosis induction. The recovery of ALDH1A3 expression appeared to be regulated by EGFR-dependent PI3K pathway activation since Akt was activated only in ALDH1A3 high clones. Blocking the EGFR signaling pathway with the EGFR inhibitor AG1498 decreased the expression of ALDH1A3. These findings shed light on the potential application of RSL3 in the treatment of glioblastoma relapse. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Interventions of Glioma)
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13 pages, 3574 KiB  
Article
Tumor Treating Fields Alter the Kinomic Landscape in Glioblastoma Revealing Therapeutic Vulnerabilities
by Amber B. Jones, Taylor L. Schanel, Mikayla R. Rigsby, Corinne E. Griguer, Braden C. McFarland, Joshua C. Anderson, Christopher D. Willey and Anita B. Hjelmeland
Cells 2023, 12(17), 2171; https://doi.org/10.3390/cells12172171 - 30 Aug 2023
Cited by 2 | Viewed by 1397
Abstract
Treatment for the deadly brain tumor glioblastoma (GBM) has been improved through the non-invasive addition of alternating electric fields, called tumor treating fields (TTFields). Improving both progression-free and overall survival, TTFields are currently approved for treatment of recurrent GBMs as a monotherapy and [...] Read more.
Treatment for the deadly brain tumor glioblastoma (GBM) has been improved through the non-invasive addition of alternating electric fields, called tumor treating fields (TTFields). Improving both progression-free and overall survival, TTFields are currently approved for treatment of recurrent GBMs as a monotherapy and in the adjuvant setting alongside TMZ for newly diagnosed GBMs. These TTFields are known to inhibit mitosis, but the full molecular impact of TTFields remains undetermined. Therefore, we sought to understand the ability of TTFields to disrupt the growth patterns of and induce kinomic landscape shifts in TMZ-sensitive and -resistant GBM cells. We determined that TTFields significantly decreased the growth of TMZ-sensitive and -resistant cells. Kinomic profiling predicted kinases that were induced or repressed by TTFields, suggesting possible therapy-specific vulnerabilities. Serving as a potential pro-survival mechanism for TTFields, kinomics predicted the increased activity of platelet-derived growth-factor receptor alpha (PDGFRα). We demonstrated that the addition of the PDGFR inhibitor, crenolanib, to TTFields further reduced cell growth in comparison to either treatment alone. Collectively, our data suggest the efficacy of TTFields in vitro and identify common signaling responses to TTFields in TMZ-sensitive and -resistant populations, which may support more personalized medicine approaches. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Interventions of Glioma)
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Review

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19 pages, 373 KiB  
Review
The Present and Future of Optic Pathway Glioma Therapy
by Simone Dal Bello, Deborah Martinuzzi, Yan Tereshko, Daniele Veritti, Valentina Sarao, Gian Luigi Gigli, Paolo Lanzetta and Mariarosaria Valente
Cells 2023, 12(19), 2380; https://doi.org/10.3390/cells12192380 - 29 Sep 2023
Cited by 1 | Viewed by 2359
Abstract
Optic pathway gliomas (OPGs) encompass two distinct categories: benign pediatric gliomas, which are characterized by favorable prognosis, and malignant adult gliomas, which are aggressive cancers associated with a poor outcome. Our review aims to explore the established standards of care for both types [...] Read more.
Optic pathway gliomas (OPGs) encompass two distinct categories: benign pediatric gliomas, which are characterized by favorable prognosis, and malignant adult gliomas, which are aggressive cancers associated with a poor outcome. Our review aims to explore the established standards of care for both types of tumors, highlight the emerging therapeutic strategies for OPG treatment, and propose potential alternative therapies that, while originally studied in a broader glioma context, may hold promise for OPGs pending further investigation. These potential therapies encompass immunotherapy approaches, molecular-targeted therapy, modulation of the tumor microenvironment, nanotechnologies, magnetic hyperthermia therapy, cyberKnife, cannabinoids, and the ketogenic diet. Restoring visual function is a significant challenge in cases where optic nerve damage has occurred due to the tumor or its therapeutic interventions. Numerous approaches, particularly those involving stem cells, are currently being investigated as potential facilitators of visual recovery in these patients. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Interventions of Glioma)
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