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• W2514935172 startingPage "69436" @default.
• W2514935172 abstract "Vascular endothelial cell growth factor (VEGF) plays a pivotal role in promoting neovascularization. VEGF gene expression in vascular endothelial cells in normal tissues is maintained at low levels but becomes highly up-regulated in a variety of disease settings including cancers. Tumor necrosis factor superfamily 15 (TNFSF15; VEGI; TL1A) is an anti-angiogenic cytokine prominently produced by endothelial cells in a normal vasculature. We report here that VEGF production in mouse endothelial cell line bEnd.3 can be inhibited by TNFSF15 via microRNA-29b (miR-29b) that targets the 3'-UTR of VEGF transcript. Blocking TNFSF15 activity by using either siRNA against the TNFSF15 receptor known as death domain-containing receptor-3 (DR3; TNFRSF25), or a neutralizing antibody 4-3H against TNFSF15, led to inhibition of miR-29b expression and reinvigoration of VEGF production. In addition, we found that TNFSF15 activated the JNK signaling pathway as well as the transcription factor GATA3, resulting in enhanced miR-29b production. Treatment of the cells either with SP600125, an inhibitor of JNK, or with JNK siRNA, led to eradication of TNFSF15-induced GATA3 expression. Moreover, GATA3 siRNA suppressed TNFSF15-induced miR-29b expression. These findings suggest that VEGF gene expression can be suppressed by TNFSF15-stimulated activation of the JNK-GATA3 signaling pathway which gives rise to up-regulation of miR-29b." @default.
• W2514935172 created "2016-09-16" @default.
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• W2514935172 date "2016-08-29" @default.
• W2514935172 modified "2023-10-18" @default.
• W2514935172 title "TNFSF15 suppresses VEGF production in endothelial cells by stimulating miR-29b expression<i>via</i>activation of JNK-GATA3 signals" @default.
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• W2514935172 doi "https://doi.org/10.18632/oncotarget.11683" @default.
• W2514935172 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5342489" @default.
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