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RNA-seq of KYSE410 cells expressing control, USP11 or ARID1A-targeting shRNAs

ABSTRACT: We examined gene expression level in KYSE410 cells expressing control, USP11 or ARID1A-targeting shRNAs to study the mechanism underlying the tumor suppressive effect of ARID1A and USP11.

ORGANISM(S): Homo sapiens

PROVIDER: GSE132359 | GEO | 2019/11/30

REPOSITORIES: GEO

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RNA-seq of KYSE410 cells expressing control, USP11 or ARID1A-targeting shRNAs

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YM155 treated KYSE410

Project description:We used microarrays to detail the gene expression profiles of KYSE410 cell line to identify distinct up and down-regulated genes during treatment with cisplatin. KYSE410 cell line were treated with 20 nM YM155 for 6 hrs and selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to gene expression profiles of KYSE 410 cell line treated with cisplatin.

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Targeting EZH2 methyltransferase activity in ARID1A mutated cells as a synthetic lethal therapeutic strategy

Project description:ARID1A, an epigentic modifier, is often mutated in ovarian clear cell carcinoma (OCCC). In addition, EZH2 is frequently upregulated in OCCC. Inhibtion of EZH2 with an inhibitor (GSK126) selectively inhibits ARID1A-mutated cells. This study was designed to understand changes in gene expression profiles following EZH2 inhibition or ARID1A restoration. Chromatin remodelers such as ARID1A are frequently mutated in a broad array of cancers. However, targeted cancer therapy based on ARID1A mutation status has not been described. Intriguingly, ARID1A mutated cancers typically lack genomic instability, suggesting significant involvement of epigenetic mechanisms. Here we show that inhibition of the EZH2 methyltransferase acts in a synthetic lethal manner in ARID1A mutated cells. Remarkably, ARID1A mutation status correlated with response to EZH2 inhibitor. Genome-wide profiling revealed antagonistic roles of ARID1A and EZH2 in gene regulation. Further, we identified PIK3IP1 as a direct ARID1A/EZH2 target gene whose upregulation contributes to the observed synthetic lethality in the EZH2 inhibitor treated ARID1A mutated cells. Significantly, EZH2 inhibitor caused the regression of established ARID1A mutated tumors in vivo. Together, this data demonstrate a synthetic lethality between ARID1A mutation and EZH2 inhibition. They indicate that pharmacological inhibition of EZH2 represents a novel treatment strategy for ARID1A mutated cancers.

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Gene expression of KYSE410 cells with treatment of 10 uM FAK inhibitor (defactinib) for 4 hours and 24 hours

Project description:KYSE410 cells were treated with 10 uM defactinib for 4 hours and 24 hours,and KYSE410 cells were collected for gene expression analysis using Agilent SurePrint G3 Human Gene Expression v3 (8×60K) Microarray. Investigation of the critical gene of KYSE410 cells treated by defactinib.

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mRNA expression of cytokine treated KYSE410 cells

Project description:KYSE410 cells were treated with PBS, TNFα, IL1β, and LPS respectively and mRNA expression profiles were assayed by Nimblegen gene expression microarray human HG18 (12x135K) Investigation of the critical gene participating various inflammatory stimuli in the process of ESCC progression.

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mRNA expression of tumor-promoting molecules treated KYSE410 cells

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