Fig. 8From: Extracellular vesicular Wnt7b mediates HPV E6-induced cervical cancer angiogenesis by activating the β-catenin signaling pathwaySchematic diagram depicting the proposed mechanism for HPV 16/18 E6-induced CC progression from the perspective of “EV-shuttled Wnt7b acts on β-catenin signaling”. In the TME, HPV 16/18 E6 upregulated Wnt7b expression in both HPV 16/18-positive CC cells and their EVs. These Wnt7b mRNA-enriched EVs could be transferred to and internalized by recipient HUVECs and then modulate HUVECs toward more proliferative and proangiogenic behaviors by acting on β-catenin signaling, eventually facilitating CC progressionBack to article page