| Description | miR-143-3p is upregulated in the paired BM tissues as compared with that in primary cancer tissues. m6A methyltransferase Mettl3 can increase the splicing of precursor miR-143-3p to facilitate its biogenesis. It targets the three binding sites of 3’UTR of vasohibin-1 (VASH1) to inhibit its expression. Mechanistically, VASH1 can increase the ubiquitylation of VEGFA to trigger the proteasome mediated degradation, further, it can endow the tubulin depolymerization through detyrosination to increase the cell motility. Thus, miR-143-3p by inhibiting VASH1 t can increase the invasion capability and angiogenesis of lung cancer |