Additional file 2 of PTEN regulates invasiveness in pancreatic neuroendocrine tumors through DUSP19-mediated VEGFR3 dephosphorylation
- Tsung-Ming Chang (575822)
- Pei-Yi Chu (285107)
- Hui-You Lin (6575792)
- Kuo-Wei Huang (1398064)
- Wen-Chun Hung (303185)
- Yan-Shen Shan (424776)
- Li-Tzong Chen (388257)
- Hui-Jen Tsai (14068117)
Publication date
November 2022
DOIAbstract
Additional file 2: Figure S2. VEGFR3 phosphorylation is responsible for pNET cell invasiveness in a VEGFC-independent manner. (A) The relative migration and invasion abilities of NIT-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 = 0.030; Wilcoxon rank-sum test. (B) The protein level of phosphorylated VEGFR3 in NIT-1 cells with and without knockdown of PTEN and treated with the VEGFR3-Fc chimera protein R3-Fc or the VEGFR3 inhibitor MAZ51
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