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Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [meRIP-Seq]

ABSTRACT: Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [meRIP-Seq]

PROVIDER: PRJNA1004271 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25601850_1.fastq.gz	Fastqsanger.gz
	SRR25601850_2.fastq.gz	Fastqsanger.gz
	SRR25601851_1.fastq.gz	Fastqsanger.gz
	SRR25601851_2.fastq.gz	Fastqsanger.gz
	SRR25601852_1.fastq.gz	Fastqsanger.gz

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Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [meRIP-Seq]

Project description:The N6-methyladenosine (m6A) RNA modification is an important regulator of gene expression. m6A is deposited by a methyltransferase complex that includes methyltransferase-like 3 (METTL3) and methyltransferase-like 14 (METTL14). High levels of METTL3 and METTL14 drive the growth of many types of adult cancer, and METTL3/METTL14 inhibitors are emerging as new anticancer agents. However, little is known about the m6A epitranscriptome or the role of the METTL3/METTL14 complex in neuroblastoma, a common pediatric cancer. Here, we show that METTL3 knockdown or pharmacologic inhibition with the small molecule STM2457 leads to reduced neuroblastoma cell proliferation and increased differentiation. These changes in neuroblastoma phenotype were associated with decreased m6A deposition on transcripts involved in nervous system development and neuronal differentiation and increased stability and expression of target mRNAs. In preclinical studies, STM2457 treatment suppressed the growth of neuroblastoma tumors in vivo. Together, these results support the potential of METTL3/METTL14 complex inhibition as therapeutic strategy against neuroblastoma.

2024-04-10 | GSE240582 | GEO

Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [RNA-Seq STM]

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Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [RNA-Seq Decay]

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Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [RNA-seq siMETTL3]

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Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation

Project description:Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation

| PRJNA1004276 | ENA

Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [RNA-Seq Decay]

Project description:Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [RNA-Seq Decay]

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Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [RNA-Seq STM]

Project description:Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [RNA-Seq STM]

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Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [RNA-seq siMETTL3]

Project description:Small-molecule Inhibition of METTL3 Suppresses Tumor Growth and Promotes Neuroblastoma Differentiation [RNA-seq siMETTL3]

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MeRIP-seq to explore the targets of METTL3 in pancreatic cancer

Project description:We performed MeRIP-seq of METTL3-knockdown (KD) MIAPaCa-2 and control cells to detect METTL3-methylated genes and extracted genes whose methylation was lost in METTL3-KD cells compared with control cells. Next, we performed mRNA expression analysis using dates of input samples at MeRIP-seq. Genes whose methylation peaks were abolished by METTL3-KD and whose expression changes were observed were analyzed as candidates for METTL3-regulated genes.

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Project description:To investigate whether the role of METTL3 in hNPCs is dependent on its m6A activity,samples form neural progenitor cell (NPC) differentiation in the small molecule-assisted shut-off (SMASh) tagged hESC groups were collected. Gene expression levels were quantitated by RNA-seq analysis, and the potential target genes were identified by MeRIP-seq analysis and RIP-seq.

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