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Effect of HSD52 overexpression on gene expression in LN229 glioma cells

ABSTRACT: Effect of HSD52 overexpression on gene expression in LN229 glioma cells

PROVIDER: PRJNA1034052 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26617840_1.fastq.gz	Fastqsanger.gz
	SRR26617840_2.fastq.gz	Fastqsanger.gz
	SRR26617841_1.fastq.gz	Fastqsanger.gz
	SRR26617841_2.fastq.gz	Fastqsanger.gz
	SRR26617842_1.fastq.gz	Fastqsanger.gz

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Effect of HSD52 overexpression on gene expression in LN229 glioma cells

Project description:In order to study the effect of HSD52 on the malignant progression and chemotherapy resistance of glioma, we examined the effect of HSD52 on the gene expression of brain glioma cells. We used lentiviral constructs to establish the LN229 cell line overexpressing HSD52. We subsequently performed gene expression profiling using RNA-seq data obtained from control LN229 cells and HSD52-overexpressing LN229 cells.

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Project description:Overexpression of histone deacetylases (HDACs) in cancer commonly causes resistance to genotoxic based therapies. Here we report on the novel mechanism whereby overexpressed class I HDACs increase the resistance of glioblastoma cells to the SN1 methylating agent temozolomide (TMZ). The chemotherapeutic TMZ triggers the activation of the DNA damage response (DDR) in resistant glioma cells, leading to DNA lesion bypass and cellular survival. Mass spectrometry analysis revealed that the catalytic activity of class I HDACs stimulates the expression of the E3 ubiquitin ligase RAD18. Furthermore, the data show that RAD18 is part of the O6-methylguanine-induced DDR as TMZ induces the formation of RAD18 foci at sites of DNA damage. Downregulation of RAD18 by HDAC inhibition prevents glioma cells from activating the DDR upon TMZ exposure. Lastly, RAD18 or O6-methylguanine-DNA methyltransferase (MGMT) overexpression abolishes the sensitization effect of HDAC inhibition on TMZ-exposed glioma cells. Our study describes the mechanism whereby class I HDAC overexpression in glioma cells causes resistance to TMZ treatment. HDACs accomplish this by promoting the bypass of O6-methylguanine DNA lesions via enhancing RAD18 expression. It also provides a treatment option with HDAC inhibition to undermine this mechanism.

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Alternative Reading Frame (ARF) overexpression in LN229 glioma cells

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miR-139-5p induced gene expression alteration in glioma cells

Project description:To evaluate gene expression alteration following miR-139-5p transfection in glioma cells. We find a significant downregulation of two transcriptional factors, E2F3 and HoxA9. Total RNA were extracted from U87, LN229 and U251 glioma cells transfected with miR-139-5p or miRNA negative control.

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Project description:Knockdown of Sox2 in LN229 gliomal cancer cells decrease their growth rates in vitro. We used microarrays to detail the global programme of gene expression in Sox2 Knockdown LN229 cells compared with mock knockdown LN229 cells Sox2 knockdown LN229 cells and and mock knockdown LN229 cells were cultured in DMEM cell culture media for RNA extraction and hybridization on Applied Biosystems Human Genome Survey Microarrays . We sought to obtain the genes regulated by Sox2 in glioma cell line.

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