This intervention effectively reduced TNS1 expression and suppressed the progression of HCC in a mouse model. Collectively, our findings underscore the therapeutic potential of targeting the GFAT1-VEZF1-TNS1 signaling axis in HCC.
However, administration of GFAT1-overexpressing BCa cells-derived sEVs increase the angiogenetic activity in the ECs of GFAT1-knockout mice. In summary, this study suggests that inhibiting sEV-mediated GFAT1 secretion from BCa cells and targeting SerRS O-GlcNAcylation in ECs may serve as novel strategies for BCa antiangiogenetic therapy.