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

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.

Intra-tumour molecular heterogeneity of clear cell renal cell carcinoma reveals the diversity of the response to targeted therapies using patient-derived xenograft models.

Inter- and intra-tumour molecular heterogeneity is increasingly recognized in clear cell renal cell carcinoma (ccRCC). It may partially explain the diversity of responses to targeted therapies and the various clinical outcomes. In this study, a 56-year-old male ccRCC patient with multiple metastases received radical nephrectomy and resection of the metastatic tumour in chest wall.

Vascular Endothelial Growth Inhibitor, a Cytokine of the Tumor Necrosis Factor Family, is Associated With Epithelial-Mesenchymal Transition in Renal Cell Carcinoma.

Previous studies have revealed that the activation of the epithelial-mesenchymal transition (EMT) endows metastatic properties upon cancer cells to promote invasion and migration. In this study, immunohistochemical analysis was performed in 50 cases of clear cell renal cell carcinoma (RCC) and paired normal kidney tissues. We detected the expression of vascular endothelial growth inhibitor (VEGI) and EMT markers (E-cadherin, fibronectin, and Slug) and recorded the clinical, pathologic, and follow-up (median follow-up: 79.

Cobalt Chloride-induced Hypoxia Induces Epithelial-mesenchymal Transition in Renal Carcinoma Cell Lines.

Objective: To establish epithelial-mesenchymal transition (EMT) models in renal cell carcinoma (RCC) cell lines.

Materials And Methods: The RCC cell lines A498 and 786-O were used in the experiment and CoCl was used to simulate hypoxia. Cells were cultured with different concentrations of CoCl.

Vascular endothelial growth inhibitor 174 is a negative regulator of aggressiveness and microvascular density in human clear cell renal cell carcinoma.

Aims: To evaluate the role and expression of vascular endothelial growth inhibitor isoform 174 (VEGI 174) in the microvessels and its correlation with microvessel density (MVD) and prognosis of clear cell renal cell carcinoma (CCRCC).

Materials And Methods: Immunohistochemical analysis was performed in 98 cases of renal cell carcinoma and paired normal kidney tissues for VEGI 174 and CD34. The clinical, pathological and follow-up (median follow-up: 54.

Suppression of renal cell carcinoma growth in vivo by forced expression of vascular endothelial growth inhibitor.

Vascular endothelial growth inhibitor (VEGI) has been associated with tumor-related vasculature in certain malignancies. However, its implication in renal cell carcinoma (RCC), an angiogenesis-dependent tumor, remains unknown. In the present study, we investigated the role played by VEGI in RCC.

The differential expression of vascular endothelial growth inhibitor isoforms, VEGI251, VEGI174 and VEGI192 in human clear-cell renal cell carcinoma.

Unlabelled: Vascular endothelial growth inhibitor (VEGI) is a recently identified antiangiogenic cytokine that belongs to the tumour necrosis factor (TNF) superfamily, and may be essential for many physiological and pathological processes. However, the expression of VEGI and in particular its isoforms, VEGI251, VEGI192 and VEGI174, in clear-cell renal cell carcinoma (CCRCC) remain unknown. In the current study, we investigated the expression of the three isoforms of VEGI in CCRCC.