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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

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

Fig. 8

YAP1 enhances the stability of HIF1A upon nicotine treatment. a-b, qRT-PCR assays of the mRNA level of HIF1A in Panc-1 (a) and BxPC3 (b) cells after transfection with the indicated vectors in the absence or presence of Nic. c-d,, Western blot assays of the protein level of HIF1A in Panc-1 (c) and BxPC3 (d) cells after transfection with the indicated vectors in the absence or presence of Nic. e, After transfection with siYAP1, western blot assays of the protein level of HIF1A in cycloheximide (CHX, 100 μg/mL) treated Panc-1 cells at the different time points upon Nic treatment. f, After transfection with siYAP1, western blot assays of the protein level of HIF1A in MG132 (10 μM) treated Panc-1 cells upon nicotine treatment. g, Diagram depicts the proposed pathway involved in YAP1-mediated PDAC progression in response to nicotine. Nic, nicotine; n.s., not significant; CHRNA, cholinergic receptor nicotinic alpha. *p < 0.05, **p < 0.01

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