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E-GEOD-7835

ABSTRACT: Transcription profiling by array of human glioblastoma cells after stimulation with deferoxamine and treatment with polyamide 1, echinomycin, or HIF-1a siRNA

OTHER RELATED OMICS DATASETS IN: PRJNA100075

PROVIDER: E-GEOD-7835 | ExpressionAtlas | 2025-01-24

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-7835-analysis-methods.tsv	Tabular
	E-GEOD-7835-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-7835-configuration.xml	Xml
	E-GEOD-7835-percentile-ranks.tsv	Tabular
	E-GEOD-7835.condensed-sdrf.tsv	Tabular

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Project description:Brusatol (Bru), a Chinese herbal extract, has a variety of anti-tumor effects. However, little is known regarding its role and underlying mechanism in glioblastoma cells. Here, we found that Bru could inhibit the proliferation of glioblastoma cells in vivo and in vitro. Besides, it also had an inhibitory effect on human primary glioblastoma cells. In order to further study the underlying mechanism of Bru’s action on GBM, we performed RNA sequencing array on GBM cells treated by Bru with IC50 for 48 hours. A log2 fold change >1.0 and a P < 0.05 were used as cutoff criteria. The volcano plots results showed that Bru significantly changed the mRNA expression pattern in U251 (819 upregulated genes and 954 downregulated genes) and U87 (485 upregulated genes and 266 downregulated genes) cells. Then, we subjected these differentially expressed genes to the Reactome pathway database (https://reactome.org), which provides molecular details of signal transduction, transport, DNA replication, metabolism, and other cellular processes as an ordered network of molecular transformations in a single, consistent data model. Reactome enrichment analysis indicated that the collagen and extracellular matrix related pathways (Italic Script with *) were mainly involved in Bru-treated GBM cells. Subsequently, we used the Venn diagram analysis (VDA) to display the shared genes between U251 and U87 cells and finally determined that ESM1, an important factor in extracellular matrix formation, changed obviously by Bru treatment. Down-regulating the expression of ECM1 via transfecting siRNA could weaken the proliferation and invasion of glioblastoma cells and promote the inhibitory effect of Bru treatment. Lentivirus-mediated overexpression of ECM1 could effectively reverse this weakening effect. Our findings indicated that Bru could inhibit the proliferation and invasion of glioblastoma cells by suppressing the expression of ECM1, and Bru might be a novel effective anticancer drug for glioblastoma cells.

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E-GEOD-7835

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