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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

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

Fig. 5

Extracellular vesicular Wnt7b mediates the HPV 16/18 E6-induced proliferation and angiogenesis of HUVECs through β-catenin signaling. a The transcriptional activity of β-catenin was assessed using the TOP/FOP dual-luciferase reporter system. The results showed that HUVECs treated with EV/E6-KD derived from the four HPV 16/18-positive CC cell lines exhibited less transcriptional activity of β-catenin than corresponding controls, while treatment with EV/E6-KD + Wnt7b-OE restored the transcriptional activity of β-catenin in HUVECs. b Western blot analysis of nuclear and total β-catenin expression in HUVECs treated with EV/NC, EV/E6-KD or EV/E6-KD + Wnt7b-OE derived from the 4 HPV 16/18-positive CC cell lines. c CCK8 proliferation assay with HUVECs. HUVECs were treated with EVs derived from the 4 HPV 16/18-positive CC cell lines in the presence or absence of FH535, an inhibitor of Wnt/β-catenin signaling. d Tube formation by HUVECs. HUVECs were treated with EVs derived from the 4 HPV 16/18-positive CC cell lines in the presence or absence of FH535. Left: representative photographs illustrating the dynamics of the angiogenic behavior of HUVECs. Right: the relative tube lengths in HUVEC cultures. * P < 0.05, ** P < 0.01

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