METTL5 deficiency induces lung cancer regression via mitochondrial translation reduction

Cellular protein synthesis occurs through two types of translation: cytoplasmic and mitochondrial. These two types of translation operate independently but in coordination to regulate cell survival and death. Methyltransferase-like 5 (METTL5) has been found to play a role in directing the m6A modification of rRNA, which in turn controls cytoplasmic translation and impacts the decisions related to cell fate. In this study, we employed Ribo-seq to explore the effects of METTL5 deficiency on both cytoplasmic and mitochondrial translation. To investigate the potential role of METTL5 in the regulation of non-small cell lung cancer, a stable METTL5 knockout cell line was initially constructed using classical A549 and H1299 NSCLC cells using a CRISPR Cas9 sgRNA-based gene interference method.