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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Protease-activated receptor-1 (PAR1) promotes epithelial-endothelial transition through Twist1 in hepatocellular carcinoma

Fig. 3

PAR1 promoted VM formation in vitro through Twist1. a and (b) The transcriptional regulatory activities of AP1, STAT3, NF-κB, and MYC (a) and Twist1, Twist2, Snail1 and Slug (b) were measured with the Dual-luciferase Reporter Assay and data was collected with the Luminoskan Ascent Reader System. PAR1 overexpression in PLC-PRF-5 cells significantly increased the transcriptional regulatory activities of AP1, STAT3, NF-κB, and MYC (a) and the transcriptional activities of Twist1, Twist2, Snail1 and Slug (b). c The expression levels of endothelial and mesenchymal markers of PLC-PRF-5 cells were examined by Western blot when transfected with vectors of pcDNA3.1-PAR1 or pcDNA3.1-Twist1, pcDNA3.1-PAR1/pcDNA3.1-Twist1 and pcDNA3.1-PAR1/pRNAT-U6-siTwist1, respectively. d The number of VM tubes in Matrigel was increased when PAR1 was overexpressed in PLC-PRF-5 cell lines and decreased after Twist1 was knocked down in HepG2/M- and PAR1 overexpressing PLC-PRF-5 cells. e PAR1 overexpression can increase the transcriptional activities of VEGFR1, VEGFR2, and VE-cadherin, while Twist1 knockdown decreased the promotional effects in PAR1 overexpressing PLC-PRF-5 cells and high PAR1-expressing HepG2/M cells. (mean ± sd; n = 3 in triplicate; *P < 0.05, **P < 0.01)

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