METTL16 deficiency attenuates apoptosis through translational control of extrinsic death receptor during nutrient deprivation
METTL16 is a well-characterized m6A methyltransferase that has been reported to contribute to tumorigenesis in various types of cancer. However, the effect of METTL16 on tumor progression under restricted nutrient conditions, which commonly occur in tumor microenvironment, has yet to be elucidated. Herein, our study initially reported the inhibitory effect of METTL16 depletion on apoptosis under amino acid starvation conditions. Overall design: To investigate the potential role of METTL16 under nutrient deprivation, stable METTL16-knockdown (M16-KD) cell lines were initially constructed using two classic A549 NSCLC cells,  through a shRNA-based gene interference approach.