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Novel Dopamine Receptor 3 Antagonists Inhibit the Growth of Primary and Temozolomide Resistant Glioblastoma Cells

ABSTRACT: In a study focused on the role dopamine receptor 3, we completed RNA-sequencing of D456 and JX39, glioblastoma xenograft lines after SRI-21979 or dmso treatment

ORGANISM(S): Homo sapiens

PROVIDER: GSE148740 | GEO | 2020/07/01

REPOSITORIES: GEO

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Novel Dopamine Receptor 3 Antagonists Inhibit the Growth of Primary and Temozolomide Resistant Glioblastoma Cells

Project description:Novel Dopamine Receptor 3 Antagonists Inhibit the Growth of Primary and Temozolomide Resistant Glioblastoma Cells

| PRJNA625540 | ENA

Dopamine Receptor Antagonists and Radiation Create a Metabolic Vulnerability in Mouse Models of Glioblastoma

Project description:Glioblastoma is the deadliest brain tumor in adults and the standard-of-care consists of surgery followed by radiation and treatment with temozolomide. Overall survival times for patients suffering from glioblastoma are unacceptably low indicating an unmet need for novel treatment options. Using patient-derived glioblastoma lines and mouse models of glioblastoma we tested the effect of radiation and the dopamine receptor antagonist on glioblastoma self-renewal in vitro and survival in vivo. A possible resistance mechanism was investigated using RNA-Sequencing. Treatment of glioma cells with the dopamine receptor antagonist quetiapine reduced glioma cell self-renewal in vitro and combined treatment of mice with quetiapine and radiation prolonged the survival of glioma-bearing animals. The combined treatment induced the expression of genes involved in cholesterol biosynthesis. This rendered the tumors vulnerable to simultaneous treatment with atorvastatin and further significantly prolonged the survival of the animals. Our results indicate promising therapeutic efficacy with the triple combination of quetiapine, atorvastatin and radiation treatment against glioblastoma without increasing the toxicity of radiation. With both drugs readily available for clinical use our study could be rapidly translated into a clinical trial.

2021-01-28 | GSE165624 | GEO

Dopamine Receptor Antagonists and Radiation Create a Metabolic Vulnerability in Mouse Models of Glioblastoma

Project description:Dopamine Receptor Antagonists and Radiation Create a Metabolic Vulnerability in Mouse Models of Glioblastoma

| PRJNA695232 | ENA

Study on the effects of CD44 knockdown in glioblastoma multiforme cells in combination with Temozolomide

Project description:Our goal is to investigate the effects of CD44 knockdown alone and in combination with Temozolomide on glioblastoma multiforme cells. To achieve this, we treated U251 cells that had been transfected with either shCtrl lentivirus or shCD44 lentivirus with either DMSO or Temozolomide.

2023-08-31 | GSE225869 | GEO

Proteomics of Temozolomide for Glioblastoma

Project description:Using the human glioblastoma cell line LN229, temozolomide was used to detect proteome changes and identify critical components regulating chemotherapy sensitivity.

2023-05-17 | PXD042080 | Pride

The Dopamine Receptor Antagonist TFP Prevents Phenotype Conversion and Improves Survival in Mouse Models of Glioblastoma

Project description:Glioblastoma is the deadliest adult brain cancer and all patients ultimately succumb to the disease. Radiation therapy (RT) provides survival benefit of 6 months over surgery alone but these results have not improved in decades. We report that radiation induces a glioma-initiating cell phenotype and identified trifluoperazine (TFP) as a compound that interferes with this phenotype conversion. TFP caused loss of radiation-induced Nanog mRNA expression, activation of GSK3 with consecutive post-translational reduction in p-Akt, Sox2 and -catenin protein levels. TFP did not alter the intrinsic radiation sensitivity of glioma-initiating cells (GICs). Continuous treatment with TFP and a single dose of radiation reduced the number of GICs in vivo and prolonged survival in syngeneic and patient-derived orthotopic xenograft (PDOX) mouse models of glioblastoma. Our findings suggest that combination of a dopamine receptor antagonist with radiation enhances the efficacy of RT in glioblastoma by preventing radiation-induced phenotype conversion of radiosensitive non-GICs into treatment resistant, induced GICs.

2020-03-05 | GSE146358 | GEO

Gene expression data from PNU 96415E treated human glioblastoma derived neural stem cells (GNS)

Project description:Glioblastomas grow in a rich neurochemical mileu, but targeting neurochemical signaling as a potential therapeutic avenue for these incurable tumors has been underexplored. Thus, we probed patient derived glioblastoma stem cells with a focused library of neurochemicals, to identify new therapeutic targets. Dopaminergic, serotonergic and cholinergic pathways were found to be active against glioblastoma. In particular, dopamine receptor D4 (DRD4) antagonists selectively inhibited glioblastoma growth in vitro and in vivo, in addition to showing synergistic effect with temozolomide. Small molecule or genetic antagonism of DRD4 suppressed ERK1/2 signaling and impaired autophagic flux causing accumulation of autophagic vacuoles and ubiquitinated proteins, associated with G0/G1 cell cycle arrest. These data suggest a new mechanism for treating glioblastoma through modulating dopamine DRD4 signaling. We used Affymetrix microarrays to characterize the mechanism of action for dopamine receptor D4 antagonist (PNU 96415E) in human glioblastoma derived neural stem cells. We treated the human glioblastoma derived neural stem cells (GNS cells) with PNU 96415E for period of 0h, 24h and 48h and extracted RNA for hybridaization on Affymetrix microarrary (Human gene 1.0 ST array) on two GNS lines.

2016-07-15 | E-GEOD-62714 | biostudies-arrayexpress

Gene profile of glioblastoma cells treated with y15 and temozolomide

Project description:The gene expression profiles were identified in glioblastoma cells treated with FAK inhibitor Y15, temozolomide alone or with combination of Y15 and Temozolomide DBTRG and U87 were treated with FAK inhibitor Y15 at 10 microM for 24 h; U87 cells were treated with Temozolomide 100 microM for 24 h and Y15+temozolomide at the same dose as each agent alone

2013-01-12 | E-GEOD-43452 | biostudies-arrayexpress

Cytoplasmic Proteomics for Temozolomide Resistance in Glioblastoma

Project description:TMZ resistance is one of the main reasons why treatment of glioblastoma (GBM) fails. In order to investigate the underlying mechanism associated with TMZ resistance, we conducted a cytoplasmic proteome research of U87 cells treated with TMZ for 1 week. A total of 162 DEPs including 66 up-regulated proteins and 96 down-regulated proteins were identified.

2018-10-23 | PXD007759 | Pride

Gene expression data from PNU 96415E treated human glioblastoma derived neural stem cells (GNS)

2016-07-15 | GSE62714 | GEO

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