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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

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

Fig. 1

Smoking/nicotine-induced EMT is accompanied by increased YAP1 expression in PDAC cells. a, Heatmap to illustrate the hierarchical clustering of the mRNA differential expression profiles in nicotine-treated Panc-1 cells. b-c, qRT-PCR and western blot assays of YAP1 mRNA (b) and protein (c) expression levels in Panc-1 and BxPC-3 cells after treatment with different concentrations (0, 0.1,1.0, 5.0 μM; 24 h) of Nic. d-g, qRT-PCR and western blot assays of the expression levels of EMT markers (E-cad, Vim and N-cad) in PDAC cells stimulated with DMSO or Nic (1.0 μM, 24 h) after transfection with shYAP1 in Panc-1 cells (d-e) or overexpression vectors in BxPC3 cells (f-g). h, Immunohistochemical staining and quantitative results for YAP1, E-cad and Vim in human PDAC tissue microarray from ESs and NSs (n = 173). Scale bar, 100 μm. EMT, epithelial-mesenchymal transition; TT, tumor tissues; ANT, adjacent non-cancerous tissues; ES, ever smoker; NS, never smoker; E-cad, E-cadherin; Vim, vimentin; Nic, nicotine; PDAC, pancreatic ductal adenocarcinoma. GAPDH was used as an internal reference. Data are shown as the mean ± SD of three replicates. Chi square test was used for statistical analysis. **P < 0.01, ***P < 0.001

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