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Reduced expression of vasohibin-1 is associated with clinicopathological features in renal cell carcinoma

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Abstract

Vasohibin-1(VASH1) has recently been isolated as a novel negative feedback inhibitor of angiogenesis. Several studies have demonstrated that VASH1 plays important roles in tumor angiogenesis but the role of this angiogenic inhibitor in renal cell carcinoma (RCC) has not been elucidated until now. In this study, we investigated the expression pattern of VASH1 and the association with clinicopathological features in RCC. Expression of VASH1, hypoxia-inducible factor-1α (HIF-1α), and microvessel density (MVD, labeled by CD34) was assessed by immunohistochemistry in 46 RCC specimens and 20 adjacent nontumorous renal tissues (ANRTs). Correlation between vasohibin-1 and HIF-1α, MVD, and clinicopathological features was then investigated. In RCC, VASH1 was expressed mainly in the cytoplasm and membrane of tumor cells and partly in vascular endothelial cells. In ANRT, it was mainly expressed in the cytoplasm and membrane of renal tubular epithelial cells and partly in vascular endothelial cells and glomerular mesangial cells. The expression level of VASH1 in RCC tissue was significantly lower than that in ANRT and was significantly reduced with the increased degree of malignancy in RCC tissues. In addition, a significantly negative correlation was noted between VASH1 expression and HIF-1α expression and a significantly negative correlation was noted between VASH1 expression and MVD in RCC. Therefore, VASH1 expression is reduced and it associates with clinicopathological features in RCC. Based on our findings and the knowledge of other angiogenesis inhibitors, we postulate that VASH1 would potentially be a biomarker and a candidate for molecular targeted therapy for patients with RCC in the future.

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Correspondence to Ruifa Han or Yan Sun.

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Zhao, G., Yang, Y., Tang, Y. et al. Reduced expression of vasohibin-1 is associated with clinicopathological features in renal cell carcinoma. Med Oncol 29, 3325–3334 (2012). https://doi.org/10.1007/s12032-012-0313-x

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  • DOI: https://doi.org/10.1007/s12032-012-0313-x

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