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ChIP seq of CDK6-WT and CDK6-K43M in murine BCR-ABL(p185)+ pre/pro B-cells

ABSTRACT: ChIP seq of CDK6-WT and CDK6-K43M in murine BCR-ABL(p185)+ pre/pro B-cells

PROVIDER: PRJNA1101496 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28722053.fastq.gz	Fastqsanger.gz
	SRR28722054.fastq.gz	Fastqsanger.gz
	SRR28722055.fastq.gz	Fastqsanger.gz
	SRR28722056.fastq.gz	Fastqsanger.gz
	SRR28722057.fastq.gz	Fastqsanger.gz

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Project description:The transcription factor c-JUN and its upstream kinase JNK1 have been implicated in BCR-ABL induced leukemogenesis. JNK1 has been shown to regulate BCL2 expression thereby altering leukemogenesis, but the impact of c-JUN remained unclear. In this study we show that JNK1 and c-JUN promote leukemogenesis via separate pathways, since lack of c-JUN impairs proliferation of p185BCR-ABL transformed cells without affecting viability. The decreased proliferation of c-JunD/D cells is associated with the loss of cyclin dependent kinase 6 (CDK6) expression. In c-JunD/D cells CDK6 expression becomes down-regulated upon BCR-ABL induced transformation which correlates with CpG island methylation within the 5´ region of Cdk6. We verified the impact of Cdk6 deficiency by using Cdk6-/- mice that developed BCR-ABL induced B-lymphoid leukemia with significantly increased latency and an attenuated disease phenotype. In addition we show that re-expression of CDK6 in BCR-ABL transformed c-JunD/D cells reconstitutes proliferation and tumor formation in Nu/Nu mice. In summary, our study reveals a novel function for the AP-1 transcription factor c-JUN in leukemogenesis by antagonizing promoter methylation. Moreover, we identify CDK6 as relevant and critical target of AP-1 regulated DNA methylation upon BCR-ABL induced transformation, thereby accelerating leukemogenesis.

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