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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

ABSTRACT: MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

PROVIDER: PRJNA418953 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5227180.fastq.gz	Fastqsanger.gz
	SRR5227181.fastq.gz	Fastqsanger.gz
	SRR5227182.fastq.gz	Fastqsanger.gz
	SRR5227183.fastq.gz	Fastqsanger.gz
	SRR5227184.fastq.gz	Fastqsanger.gz

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [mutant MEF2C]

Project description:In acute myeloid leukemia, chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that transgenic Mef2cS222A/S222A mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9. MEF2C phosphorylation was required for leukemia stem cell maintenance, induced by MARK kinases in cells, and blocked by selective MARK inhibitor MRT199665, which caused apoptosis of MEF2C-activated human AML cell lines and primary patient specimens, but not those lacking MEF2C. These findings identify signaling-dependent dysregulation of transcription factor control as a determinant of therapy response in AML, with immediate potential for improved diagnosis and therapy for this disease.

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [inhibitor MRT199665]

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [ATAC-seq]

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [inhibitor MRT199665]

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Project description:In acute myeloid leukemia (AML), chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that Mef2cS222A/S222A knock-in mutant mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9 MEF2C phosphorylation was required for leukemia stem cell maintenance and induced by MARK kinases in cells. Treatment with the selective MARK/SIK inhibitor MRT199665 caused apoptosis and conferred chemosensitivity in MEF2C-activated human AML cell lines and primary patient specimens, but not those lacking MEF2C phosphorylation. These findings identify kinase-dependent dysregulation of transcription factor control as a determinant of therapy response in AML, with immediate potential for improved diagnosis and therapy for this disease.Significance: Functional proteomics identifies phosphorylation of MEF2C in the majority of primary chemotherapy-resistant AML. Kinase-dependent dysregulation of this transcription factor confers susceptibility to MARK/SIK kinase inhibition in preclinical models, substantiating its clinical investigation for improved diagnosis and therapy of AML. Cancer Discov; 8(4); 478-97. ©2018 AACR.This article is highlighted in the In This Issue feature, p. 371.

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

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2018-07-23 | GSE107073 | GEO

Impact of MEF2C on chromatin accessibility of mouse BM pre-B and myeloid cells

Project description:We analyzed the chromatin accessibility of control and Mef2c deficient mouse BM pre-B and myeloid cells by ATAC-seq analysis.

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