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Rexinoids Induce Differential Gene Expression in Human Glioblastoma Cells

ABSTRACT: Rexinoids Induce Differential Gene Expression in Human Glioblastoma Cells

PROVIDER: PRJNA1126680 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29492841_1.fastq.gz	Fastqsanger.gz
	SRR29492841_2.fastq.gz	Fastqsanger.gz
	SRR29492842_1.fastq.gz	Fastqsanger.gz
	SRR29492842_2.fastq.gz	Fastqsanger.gz
	SRR29492843_1.fastq.gz	Fastqsanger.gz

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Rexinoids Induce Differential Gene Expression in Human Glioblastoma Cells

Project description:Rexinoids are compounds that bind to the rexinoid X receptor (RXR) to modulate gene expression and have been proposed as a new class of therapeutics to treat Alzheimer's disease. Different rexinoids will initiate downstream effects that can be quite marked even though such compounds can be structurally similar and have comparable RXR binding affinities. RXR can both homo- and heterodimerize and these protein-protein interactions and subsequent transactivating potential leads to differential gene expression, depending on the RXR dimeric partner, additional cofactors recruited, and downstream transcription factors that are up- or down-regulated. Expression analysis was performed in the U87 human glioblastoma cell line treated with a panel of rexinoids, and our analysis demonstrated that rexinoids with similar RXR EC50 values can have pronounced differences in differential gene expression. Negative control was ethanol, positive control was Bexarotene, and rexinoid compounds were A34, A41, A80, and A98, concentration of 1 X 10-7 M for 24 h treatment (rexinoids synthesized at Arizona State University).

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Project description:Glioblastoma cells produce and release high amounts of glutamate into the extracellular milieu and subsequently can trigger seizure in patients. Tumor-associated microglia/macrophages (TAMs), consisting of both parenchymal microglia and monocytes-derived macrophages (MDMs) recruited from the blood, are known to populate up to 1/3 of the glioblastoma tumor environment and exhibit an alternative, tumor-promoting and supporting phenotype. However, it is unknown how TAMs respond to the excess extracellular glutamate in the glioblastoma microenvironment. We investigated the expressions of genes related to glutamate transport and metabolism in human TAMs freshly isolated from glioblastoma resections. Quantitative real-time PCR analysis showed (i) significant increases in the expressions of GRIA2 (GluA2 or AMPA receptor 2), SLC1A2 (EAAT2), SLC1A3 (EAAT1), (ii) a near-significant decrease in the expression of SLC7A11 (cystine-glutamate antiporter xCT) and (iii) a remarkable increase in GLUL expression (glutamine synthetase) in these cells compared to adult primary human microglia. TAMs co-cultured with glioblastoma cells also exhibited a similar glutamatergic profile as freshly isolated TAMs except for a slight increase in SLC7A11 expression. We next analyzed these genes expressions in cultured human MDMs derived from peripheral blood monocytes for comparison. In contrast, MDMs co-cultured with glioblastoma cells compared to MDMs co-cultured with normal astrocytes exhibited decreased expressions in the tested genes except for GLUL. This is the first study to demonstrate transcriptional changes in glutamatergic signaling of TAMs in a glioblastoma microenvironment, and the findings here suggest that TAMs and MDMs might potentially elicit different cellular responses in the presence of excess extracellular glutamate.

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