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The impact of small molecule inhibition of METTL3 on normal haematopoiesis

ABSTRACT: We performed scRNA-seq on haematoietic stem and progenitor cells of healthy wild-type mice treated with the small-molecule inhibitor of METTL3, STM2457.

ORGANISM(S): Mus musculus

PROVIDER: GSE228562 | GEO | 2023/07/20

REPOSITORIES: GEO

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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.

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Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

Project description:Methyltransferase-like 3 (METTL3), a core catalytic subunit for RNA N6-methyladenosine (m6A) modification, plays a crucial role in regulating gene expression to govern various physiological and pathological processes. However, whether and how METTL3 regulates TME and anti-tumor immunity in non-small-cell lung cancer (NSCLC) remains poorly understood. To understand the function and mechanism of METTL3 in NSCLC TME, we compare the differential expression genes (DEGs) in STM2457 (METTL3 specific inhibitor) versus DMSO treated lewis lung carcinoma cells (LLC).

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