JNK Signaling Promotes Bladder Cancer Immune Escape by Regulating METTL3-Mediated m6A Modification of PD-L1 mRNA.

Unlabelled: The RNA N6-methyladenosine (m6A) writer methyltransferase-like 3 (METTL3) is upregulated in many types of cancer and promotes cancer progression by increasing expression of several oncogenes. Therefore, a better understanding of the mechanisms regulating METTL3 expression and the key targets of METTL3 in cancer cells could provide new therapeutic targets. In this study, we found that activated JNK signaling is associated with increased METTL3 expression in bladder cancer.

The mA Methylation-Regulated AFF4 Promotes Self-Renewal of Bladder Cancer Stem Cells.

The dynamic N-methyladenosine (mA) modification of mRNA plays a role in regulating gene expression and determining cell fate. However, the functions of mA mRNA modification in bladder cancer stem cells (BCSCs) have not been described. Here, we show that global RNA mA abundance and the expression of mA-forming enzyme METTL3 are higher in BCSCs than those in non-CSCs of bladder cancer (BCa) cells.