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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: A nicotine-induced positive feedback loop between HIF1A and YAP1 contributes to epithelial-to-mesenchymal transition in pancreatic ductal adenocarcinoma

Fig. 2

Knockdown of YAP1 inhibits nicotine- induced tumor growth and EMT in a xenograft model of PDAC in mice. a, Diagram depicts the overall xenograft study; b-c, The volumes (b) and weights (c) of xenograft tumors from mice in the three experimental groups. d, HE and Ki67 staining in xenograft tumor in the three experimental groups. Scale bar, 100 μm. e, Western blotting was conducted to examine E-cad, Vim, N-cad expression in the three experimental groups. f, Immunofluorescence assays of the expression levels of Vim in xenograft tumor in the three experimental groups. Scale bar, 100 μm. g, qRT-PCR assays of the expression levels of YAP target genes, CTGF, CDX2, CYR61, and CDC20 in mice xenograft tumors. EMT, epithelial-mesenchymal transition; HE, Hematoxylin and eosin, E-cad, E-cadherin; Vim, vimentin; N-cad, N-cadherin; NC, negative control; Nic, nicotine. GAPDH was used as an internal reference. Data are shown as the mean ± SD of three replicates.*P < 0.05; **P < 0.01

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