甲基转移酶
转移RNA
小分子
化学
计算生物学
癌症研究
生物
遗传学
核糖核酸
甲基化
基因
作者
A. Sapetschnig,Ben Thomas,Eliza Yankova,Harry Fischl,Andreia S. Azevedo,S.J. Bucknell,Richard Fosbeary,Sara L. Sawyer,Shelley Evans,C. Livi,B. Andrews,Jane Rogan,N. Webster,Matthew C. T. Fyfe,Konstantinos Tzelepis,Oliver Rausch
出处
期刊:ESMO open
[Elsevier BV]
日期:2024-02-01
卷期号:9: 102330-102330
标识
DOI:10.1016/j.esmoop.2024.102330
摘要
The RNA methyltransferase METTL1 in complex with the adaptor protein WDR4 is responsible for the deposition of N7-methylguanosine at position 46 (m7G46) in a subgroup of transfer RNAs (tRNAs). The m7G46 modification in tRNAs mediates their increased structural stability and elevated expression levels, which in turn enables increased translation rates of mRNAs enriched for codons matching those tRNAs. METTL1 is often found over-expressed in cancer tissue, and its gene locus is frequently amplified in tumours. Recent studies have shown that reducing METTL1 expression leads to tumour growth inhibition making METTL1 a potential novel cancer drug target. Using structure-guided medicinal chemistry we developed and optimised small molecule inhibitors of METTL1 identified through high-throughput screening. The inhibition of METTL1 was assessed by in vitro methyltransferase and cellular mechanistic assays. Binding of compounds to METTL1 was measured by a cellular target engagement assay. Cell viability dose response curves were generated using the CellTiter-Glo® (Promega) assay. Additionally, molecular changes to tRNAs were analysed by mim-tRNA-Seq, and cell cycle analyses were performed by flow cytometry or western blotting. Cell line-derived xenograft or syngeneic in vivo mouse studies were conducted to assess tumour growth inhibition. Representative compounds of two distinct chemical series exhibit METTL1 inhibition in vitro at low nanomolar concentrations while displaying high selectivity over other RNA and protein methyltransferases. Mechanistically, METTL1 inhibition leads to reduced tRNA methylation and reduced stability of a subgroup of tRNAs. In several cancer cell lines, METTL1 inhibition impairs cell proliferation and cell cycle progression accompanied by reduced expression of cell cycle regulators. In vivo, METTL1 inhibitors induce tumour growth inhibition in both immune-deficient and immune-competent mouse strains. We describe the development and characterisation of first-in-class tRNA methyltransferase inhibitors targeting METTL1. Our data provide the first proof that pharmacological inhibition of a tRNA methyltransferase affects tumour growth in animal models.
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