EXTH-50. ACUTE AND LONG-TERM RESPONSES TO QUISINOSTAT TREATMENT IN PDX MODELS OF GLIOBLASTOMA Article Swipe
Keely Orndorff
,
James McNamara
,
Costanza LoCascio
,
Connor White
,
Mariya Stavnichuk
,
Kamal Shaik
,
Tigran Margaryan
,
Artak Tovmasyan
,
Nader Sanai
,
Shwetal Mehta
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1093/neuonc/noad179.0903
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1093/neuonc/noad179.0903
BACKGROUND Histone deacetylase inhibitors (HDACi) promote reactive oxygen species production, result in DNA damage, and trigger cell fate changes. Quisinostat is a Class I-II selective HDAC inhibitor with high specificity for HDAC1. Here, we evaluated acute and long-term quisinostat treated glioblastoma (GBM) PDX tissues and glioma stem cells for increase in reactive oxygen species and cell fate change. METHODS GBM PDX models (n = 6) and multiple PDX-derived glioma stem cells were treated with quisinostat, radiation, or a combination of quisinostat and radiation. Tissue and cells were processed via LC-MS/MS, RNA-seq, qRT-PCR, immunoblotting, and immunocytochemistry assays to examine increase in cellular reactive oxygen species, oxidative stress biomarkers, and markers of stemness and differentiation. RESULTS RNA sequencing of tumor tissue revealed that chronic co-treatment with quisinostat and radiation led to increased cellular expression of oxidative stress- and neuronal-related genes compared to control group. Immunoblotting confirmed upregulation of neuronal signaling proteins in the quisinostat treated tumor tissue in vivo. qRT-PCR and LC-MS/MS analysis demonstrated an increase in oxidative stress biomarkers following acute quisinostat treatment in vitro. CONCLUSIONS Treatment with quisinostat increased the expression of genes involved in promoting oxidative stress and neuronal signaling in vivo. LC-MS/MS, qRT-PCR, immunoblotting and immunocytochemistry assays confirmed increase in oxidative stress and neuronal markers upon acute treatment in vitro. Cancer cells often express higher levels of reactive oxygen species compared to normal tissue, and oxidative stress is linked to greater survival and proliferation of cancer cells. However, there is much interest in increasing oxidative stress in glioma cells to induce selective cell death in cancer cells. Ongoing studies are aimed at evaluating the significance of these cellular and molecular changes resulting from quisinostat treatment and whether the quisinostat-induced oxidative stress and cell fate changes can be exploited for future combination therapy for GBM.
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- Type
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- Language
- en
- Landing Page
- https://doi.org/10.1093/neuonc/noad179.0903
- OA Status
- green
- Related Works
- 10
- OpenAlex ID
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All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4388590750Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1093/neuonc/noad179.0903Digital Object Identifier
- Title
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EXTH-50. ACUTE AND LONG-TERM RESPONSES TO QUISINOSTAT TREATMENT IN PDX MODELS OF GLIOBLASTOMAWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2023Year of publication
- Publication date
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2023-11-01Full publication date if available
- Authors
-
Keely Orndorff, James McNamara, Costanza LoCascio, Connor White, Mariya Stavnichuk, Kamal Shaik, Tigran Margaryan, Artak Tovmasyan, Nader Sanai, Shwetal MehtaList of authors in order
- Landing page
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https://doi.org/10.1093/neuonc/noad179.0903Publisher landing page
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YesWhether a free full text is available
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greenOpen access status per OpenAlex
- OA URL
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https://pmc.ncbi.nlm.nih.gov/articles/PMC10639519/pdf/noad179.0903.pdfDirect OA link when available
- Concepts
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Oxidative stress, Reactive oxygen species, Immunocytochemistry, Cancer research, Downregulation and upregulation, Biology, Glioma, Molecular biology, Chemistry, Cell biology, Biochemistry, Gene, EndocrinologyTop concepts (fields/topics) attached by OpenAlex
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0Total citation count in OpenAlex
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10Other works algorithmically related by OpenAlex
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| primary_location.id | doi:10.1093/neuonc/noad179.0903 |
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| primary_location.source.host_organization_name | Oxford University Press |
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| primary_location.raw_source_name | Neuro-Oncology |
| primary_location.landing_page_url | https://doi.org/10.1093/neuonc/noad179.0903 |
| publication_date | 2023-11-01 |
| publication_year | 2023 |
| referenced_works_count | 0 |
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