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Hypomethylating agents sensitize diffuse large B-cell lymphoma to venetoclax

ABSTRACT: Hypomethylating agents sensitize diffuse large B-cell lymphoma to venetoclax

PROVIDER: PRJNA926939 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23199438.fastq.gz	Fastqsanger.gz
	SRR23199439.fastq.gz	Fastqsanger.gz
	SRR23199440.fastq.gz	Fastqsanger.gz
	SRR23199441.fastq.gz	Fastqsanger.gz
	SRR23199442.fastq.gz	Fastqsanger.gz

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Hypomethylating agents sensitize diffuse large B-cell lymphoma to venetoclax

Project description:We established acquired venetoclax resistant OCI-LY1R cell line by treating venetoclax sensitive parental OCI-Ly1 cell line with increasing doses of venetoclax up till 1µM. Parental OCI-Ly1 and venetoiclax-resistant OCI-Ly1R cells were treated with vehicle control or decitabine at 1uM for 3 days. We found that decitabine differantially regulated gene expression in venetoclax sensitive and resistant cells. With gene set enrichment analysis, we identified two pathways that were deregulated by decitabine in both cell lines.

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SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents

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SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents

Project description:Large-scale sequencing efforts in Clear cell renal cell carcinoma (ccRCC) have found a high prevalence of mutations in chromatin-related genes. Prominent within this group is SETD2, which is mutated in 15% of ccRCC and is associated with aggressive disease. SETD2 is a methyltransferase responsible for trimethylating lysine 36 on histone H3 (H3K36me3). Although it is not completely understood how SETD2 loss contributes to ccRCC tumorigenesis, it is thought that it reprograms the epigenetic landscape of the cell. Here we explore the impact that SETD2/H3K36me3 loss has on the DNA methylome in ccRCC cells. DNA methylation was measured using the EPIC DNA methylation assay in 786-O ccRCC cells and non-cancerous transformed proximal tubule kidney cells (HKC) with and without SETD2. Sensitivity to DNA hypomethylating agents was assessed by dose-response assay using 5-aza-2'-deoxycytidine. Apoptosis was measured via Annexin-V/PI staining by flow cytometry. Mitochondrial fitness was evaluated by electron microscopy and flow cytometry. Moreover, activity of 5-aza-2'-deoxycytidine, a DNA hypomethylating agent, in was assessed in SETD2 WT/KO xenografts in NOD-Scid mice. SETD2 loss resulted in DNA hypermethylation in HKC cells and to a greater extent in 786-O. Dose-response assays showed that SETD2-null ccRCC cells are sensitive to 5-aza-2'-deoxycytidine. Furthermore, Annexin-V/PI staining revealed more apoptotic and necrotic cells in SETD2-null cells following 5-aza-2'-deoxycytidine treatment, which was rescued using a Caspase inhibitor. In addition, 5-aza-2'-deoxycytidine induced profound changes in mitochondria in SETD2-null cells, including loss of membrane potential and size reduction. Indeed, in vivo experiments verified increased SETD2-null xenografts’ sensitivity to 5-aza-2'-deoxycytidine. We show that SETD2 loss in ccRCC cells causes DNA hypermethylation, creating a synthetic lethal dependency with DNA hypomethylating agents.

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Project description:SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents [methylation]

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DNA hypomethylating agents increase activation and cytolytic activity of CD8+ T-cells

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