TY - JOUR T1 - 1α,25(OH)<sub>2</sub>D<sub>3</sub> Analog, MART-10, Inhibits Neuroendocrine Tumor Cell Metastasis After VEGF-A Stimulation JF - Anticancer Research JO - Anticancer Res SP - 6215 LP - 6221 VL - 37 IS - 11 AU - KUN-CHUN CHIANG AU - CHUN-NAN YEH AU - JONG-HWEI S. PANG AU - JUN-TE HSU AU - TA-SEN YEH AU - LI-WEI CHEN AU - SHENG-FONG KUO AU - MASASHI TAKANO AU - TAI C. CHEN AU - ATSUSHI KITTAKA AU - PO-JEN HSIEH AU - HORNG-HENG JUANG Y1 - 2017/11/01 UR - http://ar.iiarjournals.org/content/37/11/6215.abstract N2 - Aims: Pancreatic neuroendocrine tumors (PanNETs) are usually diagnosed in an advanced stage. Most patients with PanNETs die of metastasis. Vascular endothelial growth factor-A (VEGF-A) is a strong stimulator of angiogenesis and tumor metastasis. We aimed to investigate the effect of MART-10 [19-nor-2α-(3-hydroxypropyl)-1α,25(OH)2D3], a 1α,25-dihydroxy-vitamin D3 (1α,25(OH)2D3) analog, on PanNET cell metastasis after VEGF-A stimulation. Materials and Methods: Migration and invasion assays, western blot, and immunofluorescent staining were applied in this study. Results: VEGF-A increased PanNET cell migration and invasion, which was attenuated by 1α,25(OH)2D3 and MART-10. VEGF-A treatment stimulated epithelial–mesenchymal transition (EMT) of PanNET cells. During this process, expression of snail family transcriptional repressor 1 and 2, and fibronectin was up-regulated. 1α,25(OH)2D3 and MART-10 counteracted VEGF-A-induced EMT. In addition, expression of neuropilin 1, a key protein in VEGF-A signaling, was down-regulated by 1α,25(OH)2D3 and MART-10. Furthermore, synthesis of F-actin was increased by VEGF-A and reduced by 1α,25(OH)2D3 and MART-10. Conclusion: Our data indicate that MART-10 could be deemed a promising drug for PanNET treatment. ER -