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A novel and highly effective mitochondrial uncoupling drug (MB1-47) in T-cell acute lymphoblastic leukemia

ABSTRACT: A novel and highly effective mitochondrial uncoupling drug (MB1-47) in T-cell acute lymphoblastic leukemia

PROVIDER: PRJNA694438 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13516818_1.fastq.gz	Fastqsanger.gz
	SRR13516818_2.fastq.gz	Fastqsanger.gz
	SRR13516819_1.fastq.gz	Fastqsanger.gz
	SRR13516819_2.fastq.gz	Fastqsanger.gz
	SRR13516820_1.fastq.gz	Fastqsanger.gz

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A novel and highly effective mitochondrial uncoupling drug (MB1-47) in T-cell acute lymphoblastic leukemia

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy. Despite recent advances in treatments with intensified chemotherapy regimens, relapse rates and associated morbidities remain high. In this context, metabolic dependencies have emerged as a druggable opportunity for the treatment of leukemia. Here, we tested the antileukemic effects of MB1-47, a newly developed mitochondrial uncoupling compound. MB1-47 treatment in T-ALL cells robustly inhibited cell proliferation via both cytostatic and cytotoxic effects as a result of compromised mitochondrial energy and macromolecule depletion, which severely impair nucleotide biosynthesis. Mechanistically, acute treatment with MB1-47 in primary leukemias promoted AMPK activation and downregulation of mTOR signaling, stalling anabolic pathways that support leukemic cell survival. Indeed, MB1-47 treatment in mice harboring murine NOTCH1-induced leukemias or human T-ALL PDXs led to a potent antileukemic effect with 2-fold extension in survival without overlapping toxicities. Overall, our findings demonstrate a critical role for mitochondrial oxidative phosphorylation in T-ALL and uncover MB1-47-driven mitochondrial uncoupling as a novel therapeutic strategy for the treatment of this disease.

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