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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

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

Fig. 1

Wnt7b is highly expressed in HPV 16/18-positive CC cells and downregulated by E6 knockdown. a The expression of Wnt1, Wnt2, Wnt3a, Wnt4, Wnt5a, Wnt6, Wnt7b, Wnt10b and Wnt11 in CC cells was tested using qRT-PCR. The mRNA levels of Wnt3a, Wnt5a and Wnt7b were significantly increased in all the four HPV-positive cell lines (SiHa and CaSki cells are HPV 16 positive, while HeLa and SW756 cells are HPV 18 positive) compared to HPV-negative C33A cells. b The knockdown efficiency of HPV 16/18 E6-shRNAs in the four HPV 16/18-positive CC cell lines was analyzed using qRT-PCR. Based on the different inhibitory effects observed, we constructed stable HPV 18 E6-KD HeLa cells using HPV 18 E6-shRNA1, stable HPV 18 E6-KD SW756 cells using HPV 18 E6-shRNA3, and stable HPV 16 E6-KD SiHa and CaSki cells using HPV 16 E6-shRNA3 in the following study. c qRT-PCR analysis showed that the knockdown (KD) of HPV-E6 did not lead to a consistent expression change of Wnt3a and Wnt5a mRNA but lead to a consistently decreased Wnt7b mRNA expression in all the four HPV 16/18 positive cell lines. d Western blotting analysis showed the decreased expression of Wnt7b protein by E6-KD in all the four HPV 16/18 positive cell lines. * P < 0.05, ** P < 0.01

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