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Fig. 2 | Journal of Biomedical Science

Fig. 2

From: PTEN regulates invasiveness in pancreatic neuroendocrine tumors through DUSP19-mediated VEGFR3 dephosphorylation

Fig. 2

VEGFR3 phosphorylation is responsible for pNET cell invasiveness in a VEGFC-independent manner. A The relative migration and invasion abilities of QGP-1 cells with (shPTEN) and without (shLuc) knockdown of PTEN and treated with the VEGFR3-Fc chimera protein (shPTEN-R3Fc) or the VEGFR3 inhibitor MAZ51 (shPTEN-MAZ51). Migration: shLuc vs. shPTEN, P = 0.021; shPTEN vs. shPTEN-MAZ51, P = 0.030; Wilcoxon rank-sum test. Invasion: shLuc vs. shPTEN, P = 0.021; shPTEN vs. shPTEN-MAZ51, P = 0.029; Wilcoxon rank-sum test. B The protein level of phosphorylated VEGFR3 in QGP-1 cells with and without knockdown of PTEN and treated with the VEGFR3-Fc chimera protein or the VEGFR3 inhibitor MAZ51. C The relative migration and invasion abilities of QGP-1 cells with (shPTEN) and without (shLuc) knockdown of PTEN and with (shPTEN/VEGFR3) or without knockdown of VEGFR3. Migration: shPTEN vs. shPTEN/VEGFR3, P = 0.030; Wilcoxon rank-sum test. Invasion: shPTEN vs. shPTEN/VEGFR3, P = 0.030; Wilcoxon rank-sum test. The protein level of phosphorylated VEGFR3 in QGP-1 cells with and without knockdown of PTEN and with or without knockdown of VEGFR3 was shown in right panel

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