Protein of Vascular Endothelial Growth Inhibitor 174 Inhibits Epithelial-Mesenchymal Transition in Renal Cell Carcinoma In Vivo

• Published in: Anticancer research Vol. 37; no. 8; pp. 4269 - 4275
• Main Authors: Zhao, Qiang, Deng, Xiaohu, Hong, Baoan, Wang, Feng, Tang, Xinxin, Yang, Yong, Gong, Kan, Ye, Lin, Jiang, Wen G, Zhang, Ning
• Format: Journal Article
• Language: English
• Published: Greece 01.08.2017
• Subjects: Animals; Carcinoma, Renal Cell - drug therapy; Carcinoma, Renal Cell - genetics; Carcinoma, Renal Cell - pathology; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - drug effects; Epithelial-Mesenchymal Transition - drug effects; Gene Expression Regulation, Neoplastic - drug effects; Growth Inhibitors - administration & dosage; Humans; Mice; Tumor Necrosis Factor Ligand Superfamily Member 15 - antagonists & inhibitors; Tumor Necrosis Factor Ligand Superfamily Member 15 - biosynthesis; Tumor Necrosis Factor Ligand Superfamily Member 15 - genetics; Xenograft Model Antitumor Assays; epithelial–mesenchymal transition; Renal cell carcinoma; vascular endothelial growth inhibitor (VEGI)
• ISSN: 0250-7005; 1791-7530
• DOI: 10.21873/anticanres.11819

Vascular endothelial growth inhibitor (VEGI) is a member of the tumor necrosis factor superfamily, identified as an anti-angiogenic cytokine. However, the effect of VEGI on epithelial-mesenchymal transition (EMT) in renal cell carcinoma (RCC) is still unknown. In this study, protein VEGI174 was designed and synthesized. Renal cell carcinoma A498 cells were implanted into immune-deficient mice to establish tumor models. Two groups were included: control group treated with saline, and VEGI174-treated group. Data of tumor growth were collected every 3 to 4 days. Two weeks later, the tumor specimens were harvested for immunohistochemical staining of EMT markers (E-cadherin, N-cadherin, vimentin). Compared to the saline-treated group, the VEGI174-treated group showed significant inhibition of tumor growth (p<0.05). The expression of E-cadherin was significantly higher in the VEGI174-treated group compared to the saline-treated group (p<0.01). However, the expression of N-cadherin and vimentin were reduced in the VEGI174-treated group. Our findings indicate that VEGI174 prevents progression and tumor metastasis through inhibiting EMT in RCC in vivo. This may provide a new approach for the treatment of RCC.