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RNA-seq analysis for OVSAHO cells with upregulated SMARCA2 and downregulated SMARCA4 expression

ABSTRACT: The goal of this study is to explore the underlying mechanism which contributes to chemoresistance in high-grade serous carcinoma (HGSC) with low SMARCA4 and high SMARCA2 expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE212886 | GEO | 2023/02/07

REPOSITORIES: GEO

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ATAC-seq analysis for OVSAHO cells with upregulated SMARCA2 and downregulated SMARCA4 expression

Project description:The goal of this study is to explore the underlying mechanism which contributes to chemoresistance in high-grade serous carcinoma (HGSC) with low SMARCA4 and high SMARCA2 expression.

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Project description:Using ATAC-seq, we identified the accessibility changes in lung cancer cells (NCI-H1944) reconstituted with SMARCA4 WT or SMARCA4 mutants. We also determined the SMARCA2-regulated accessibility program in NCI-H1944 after SMARCA2 depletion. Lastly, we identified the SMARCA2 accessibility program that is rescued by SMARCA4 WT and mutants. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech.

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Project description:Pharmacological inhibition of the SMARCA4 bromodomain inhibited human leukemic cell proliferation, phenocopying SMARCA4 knockdown in these cells. We performed microarray analysis of global gene expression changes in MV4-11 cells after 6 days of PFI-3 treatment and after SMARCA4 knock-down. With this analysis we identified several genes whose expression was similarly up- or down-regulated upon inhibitor treatment and SMARCA4 depletion. Human acute monocytic leukemia cells (MV4-11, ACC 102) were lentivirally transduced with shRNA taregting SMARCA4 (KD) or with a negative control shRNA (Scr). In a parallel experiment MV4-11 cells were treated for 6 days with 10 uM PFI-3, which is SMARCA4, SMARCA2 and PBRM1 bromodomain inhibitor, or DMSO as a negative control. All sample types were prepared in triplicates.

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