Vascular endothelial growth inhibitor 174 and its functional domains inhibit epithelial-mesenchymal transition in renal cell carcinoma cells in vitro

Zhang,Ning; Hong,Baoan; Lian,Wenyong; Zhou,Changhua; Chen,Siqi; Du,Xin; Deng,Xiaohu; Duoerkun,Shayiremu; Li,Qing; Yang,Yong; Gong,Kan

doi:10.3892/ijmm.2017.3033

Vascular endothelial growth inhibitor 174 and its functional domains inhibit epithelial-mesenchymal transition in renal cell carcinoma cells in vitro

Authors:
- Ning Zhang
- Baoan Hong
- Wenyong Lian
- Changhua Zhou
- Siqi Chen
- Xin Du
- Xiaohu Deng
- Shayiremu Duoerkun
- Qing Li
- Yong Yang
- Kan Gong
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Affiliations: Department of Urology, Peking University Cancer Hospital, Beijing Institute for Cancer Research, Beijing 100142, P.R. China, Department of Urology, Peking University First Hospital, Beijing 100034, P.R. China, Department of Urology, Xinjiang Production and Construction Corps First Division Hospital, Aksu, Xinjiang 843000, P.R. China, School of Pharmaceutical Sciences, Center for Cellular and Structural Biology, Sun Yat-Sen University, Guangzhou, Guangdong 510006, P.R. China, Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China, Department of Urology, Karamay People's Hospital, Karamay, Xinjiang 834000, P.R. China, Department of Urology, Hami District Central Hospital, Hami, Xinjiang 839000, P.R. China
Published online on: June 19, 2017 https://doi.org/10.3892/ijmm.2017.3033
Pages: 569-575

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Abstract

The present study was carried out to investigate the effects of vascular endothelial growth inhibitor 174 (VEGI174) and its functional domains (V7 and V8) on epithelial‑mesenchymal transition (EMT) in renal cell carcinoma (RCC) cells in vitro. The RCC cell lines A498 and 786‑O were used in this study. Based on our preliminary study, we selected full‑length VEGI174 and its functional domains (V7 and V8) as the target genes in this study. Plasmids containing VEGI174, V7 or V8 transgenes were constructed and transfected into A498 and 786‑O cell lines. Cytological activity was tested during cell culture. Quantitative PCR and western blot analysis were performed to determine the expression levels of EMT markers (E‑cadherin, vimentin, β‑catenin and Slug). Overexpression of VEGI174, V7 or V8 did not have a significant influence on cell viability (P>0.05). The mRNA level of E‑cadherin was significantly upregulated, while that of vimentin was downregulated in A498VEGIexp, A498V7exp, A498V8exp, 786‑OVEGIexp, 786‑OV7exp and 786‑OV8exp cells compared with the cells containing the empty plasmid controls (P<0.05). The western blot results showed that changes in protein expression levels were consistent with the changes in mRNA expression. Both the mRNA and protein expression levels of β‑catenin and Slug were downregulated in the A498VEGIexp, A498V7exp, A498V8exp, 786‑OVEGIexp, 786‑OV7exp and 786‑OV8exp cells. In conclusion, overexpression of VEGI174, V7 or V8 inhibited EMT in A498 and 786‑O cells. Notably, V7 and V8 are two effective functional domains of VEGI174 that have the potential to be studied for peptide synthesis and the treatment of RCC.

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