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Effect of venetoclax, tedizolid, and combination treatment on gene expression in a venetoclax-resistant AML cell line

ABSTRACT: Effect of venetoclax, tedizolid, and combination treatment on gene expression in a venetoclax-resistant AML cell line

PROVIDER: PRJNA560975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10004505_1.fastq.gz	Fastqsanger.gz
	SRR10004505_2.fastq.gz	Fastqsanger.gz
	SRR10004506_1.fastq.gz	Fastqsanger.gz
	SRR10004506_2.fastq.gz	Fastqsanger.gz
	SRR10004507_1.fastq.gz	Fastqsanger.gz

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Effect of venetoclax, tedizolid, and combination treatment on gene expression in a venetoclax-resistant AML cell line

Project description:The goal of this study was to profile the changes in gene expression in an AML cell line with acquired resistance to venetoclax in response to treatment with venetoclax, tedizolid, or combination of the 2 drugs.

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Targeting mitochondrial structure sensitizes AML to Venetoclax

Project description:The BCL-2 family plays important roles in acute myeloid leukemia (AML) and Venetoclax, a selective BCL-2 inhibitor, has received FDA approval for treatment of AML. However, drug resistance ensues after prolonged treatment, highlighting the need for a greater understanding of the underlying mechanisms. Using a genome-wide CRISPR/Cas9 screen in human AML, we identified genes whose inactivation sensitizes AML blasts to Venetoclax. Genes involved in mitochondrial organization and function were significantly depleted throughout our screen, including the mitochondrial chaperonin CLPB. We demonstrated that CLPB is upregulated in human AML, it is further induced upon acquisition of Venetoclax resistance and its ablation sensitizes AML cells to Venetoclax. Mechanistically, CLPB maintains the mitochondrial cristae structure via its interaction with the cristae-shaping protein OPA1, whereas its loss promotes apoptosis by inducing cristae remodeling and mitochondrial stress responses. Overall, our data suggest that targeting mitochondrial architecture may provide a promising approach to circumvent Venetoclax resistance.

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Targeting mitochondrial structure sensitizes AML to Venetoclax

Project description:Targeting mitochondrial structure sensitizes AML to Venetoclax

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