Vasohibin‐2 is required for epithelial–mesenchymal transition of ovarian cancer cells by modulating transforming growth factor‐β signaling

• DOI: 10.1111/cas.13157
• Publication Date: 2017-01-08T11:32:39Z
• Authors: Rie Norita; Yasuhiro Suzuki; Yutaka Furutani; Kazuki Takahashi; Yasuhiro Yoshimatsu; Katarzyna A. Pody...; Tetsuro Watabe; Yasufumi Sato
• Keywords: Homeodomain Proteins; Ovarian Neoplasms; 0303 health sciences; Epithelial-Mesenchymal Transition; Neovascularization, Pathologic; Receptor, Transforming Growth Factor-beta Type I; Original Articles; Protein Serine-Threonine Kinases; Cadherins; Fibronectins; 3. Good health; Repressor Proteins; 03 medical and health sciences; Cell Line, Tumor; Plasminogen Activator Inhibitor 1; Humans; Matrix Metalloproteinase 2; Female; RNA Interference; Angiogenic Proteins; Phosphorylation; RNA, Small Interfering; Receptors, Transforming Growth Factor beta; Cell Proliferation

Vasohibin‐2 ( VASH 2) is a homolog of 1, an endothelium‐derived angiogenesis inhibitor. mainly expressed in cancer cells, and has been implicated the progression by inducing tumor growth. Although 2 recently reported to be involved epithelial–mesenchymal transition EMT ), its precise roles are obscure. The aim present study was clarify role cells relation transforming growth factor‐β TGF ‐β) signaling, which major stimulator . Decreased expression ovarian significantly repressed ‐β type I receptor, namely activin receptor‐like kinase 5. Transforming factor‐β1‐induced phosphorylation Smad2 Smad3 markedly decreased knockdown while unchanged. Accordingly, responses ‐β1 shown promoter assay plasminogen activator inhibitor 1 were attenuated cells. Furthermore, abrogated ‐β1‐induced reduced epithelial markers including E‐cadherin, elevated mesenchymal fibronectin, ZEB 2, Snail2, suggesting that endogenous required for In accordance with these results, effects on cell morphology, migration, invasion, MMP also when knocked down. These results indicate played significant modulating signaling. We propose would novel molecular target prevention cancers.