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TAL1 hijacks MYCN enhancer that induces MYCN expression and dependence on mevalonate pathway in T-cell acute lymphoblastic leukemia

ABSTRACT: TAL1 hijacks MYCN enhancer that induces MYCN expression and dependence on mevalonate pathway in T-cell acute lymphoblastic leukemia

PROVIDER: PRJNA970311 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24467507_1.fastq.gz	Fastqsanger.gz
	SRR24467507_2.fastq.gz	Fastqsanger.gz
	SRR24467508_1.fastq.gz	Fastqsanger.gz
	SRR24467508_2.fastq.gz	Fastqsanger.gz
	SRR24474808_1.fastq.gz	Fastqsanger.gz

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TAL1 hijacks MYCN enhancer that induces MYCN expression and dependence on mevalonate pathway in T-cell acute lymphoblastic leukemia

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Project description:Purpose: Identify new targets in MYCN-amplified Neuroblastoma Methods: ChIP-Seq experiments were performed on Kelly and LAN-1 neuroblastoma cells by using the following antibodies: anti-EZH2 (Cell Signaling 5246S); anti-H3K27me3 (Millipore 07-449); anti-H3K4me3 (Abcam ab8580). We evaluated the global EZH2 PRC2-dependence by identifiying direct genome-wide target genes for EZH2, H3K27me3 and H3K4me3. Results: We found that EZH2 serves a PRC2-dependent function in neuroblastoma, repressing neuronal differentiation. Moreover, EZH2-regulated genes were strongly repressed in MYCN-amplified and high-risk primary tumors. Conclusion: Our study supports testing EZH2 inhibitors in patients with MYCN-amplified neuroblastoma.

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Project description:MYCN is a common oncogenic alteration in tumors, representing one of the high-risk molecular subtypes of tumors. However, the functional role of MYCN in tumorigenesis remains to be elucidated. Here, we report that MYCN binds to the UBE2C promoter and upregulates its transcription, accelerating the progression of neuroectodermal tumor. The proteomic analysis of UBE2C-interacting proteins revealed TFRC, a well-known tumor suppressor, is a novel ubiquitin target of UBE2C. Subsequently, immunoprecipitation assay demonstrates UBE2C downregulate TFRC expression via ubiquitinoylation in neuroectodermal tumor. Suppression of UBE2C in tumor cells induced ferroptosis and increased sensitivity to the ferroptosis inducer erastin. Taken together, our findings reveal a novel MYCN-UBE2C-TFRC-ferroptosis regulatory cascade in controlling MYCN activation cell proliferation and tumor growth, pinpointing an unprecedented mechanism of MYCN-mediated evasion of ferroptosis escape in tumor. This study provides useful insights into the theoretical underpinning for therapy of MYCN activation tumors.

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