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Assessing DNA methylation differences upon aquired Venetoclax resistance

ABSTRACT: Assessing DNA methylation differences upon aquired Venetoclax resistance

PROVIDER: PRJNA701295 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13681226_1.fastq.gz	Fastqsanger.gz
	SRR13681226_2.fastq.gz	Fastqsanger.gz
	SRR13681227_1.fastq.gz	Fastqsanger.gz
	SRR13681227_2.fastq.gz	Fastqsanger.gz
	SRR13681228_1.fastq.gz	Fastqsanger.gz

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Assessing DNA methylation differences upon aquired Venetoclax resistance

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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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Project description:Resistance to the first approved BCL-2 inhibitor venetoclax is emerging in lymphoid malignancies. The study aimed to identify the genetic determinants of such resistance. From genome-scale screens we determined the genes influencing the sensitivity to BCL-2 inhibition. The present set of data is related to expression changes (assessed by RNA sequencing) observed in the resistant OCI-Ly1 lymphoma cell line as well as those resulting from genetic perturbation (using CRISPR-Cas9) targeting the genes highlighted in our genome-scale screen.

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