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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: Extracellular vesicular Wnt7b mediates HPV E6-induced cervical cancer angiogenesis by activating the β-catenin signaling pathway

Fig. 8

Schematic 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 progression

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