Abstract
Vasohibin-1(VASH1) has recently been isolated as a novel 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. We previously reported that VASH1 expression is reduced and is associated with clinicopathological features in RCC. In the present study, we investigated the biological effects of VASH1 in RCC by evaluating the effects of VASH1 on cell proliferation, cell cycle distribution, cell apoptosis and cell invasion in human umbilical vein endothelial cells (HUVECs) and 786-0 cells, and evaluating the effect of VASH1 on the growth of 786-0 cells in nude mice. A pReceiver-M61-VASH1 was transfected into HUVECs and 786-0 cells, and the expression level of VASH1 protein was examined by western blotting. Cell proliferation was detected by MTT assay, and cell cycle and apoptosis of HUVECs and 786-0 cells were analyzed by flow cytometry. The invasive ability of 786-0 cells was tested by Transwell assay. Finally, nude mouse models were established to evaluate the therapeutic effect of VASH1. The pReceiver-M61-VASH1 effectively induced the expression of VASH1 in HUVECs and 786-0 cells. VASH1 overexpression effectively inhibited cell proliferation, arrested the cell cycle in the G0/G1phase and promoted cell apoptosis of HUVECs and 786-0 cells. VASH1 overexpression effectively inhibited the subcutaneous growth of 786-0 tumors invivo. Therefore, VASH1 is a potential molecular-targeted therapy for patients with RCC.
Highlights
Renal cell carcinoma (RCC) is the most common neoplasm of the kidney in adults accounting for ~2-3% of all adult malignancies and 80-90% of primary malignant renal tumors [1,2]
To evaluate whether the recombinant plasmids were successfully transfected into the human umbilical vein endothelial cells (HUVECs) and 786-0 cells and whether VASH1 protein was expressed, we investigated the protein expression of VASH1 in HUVECs and 786-0 cells after transfection with pReceiver-M61-VASH1
In the 786-0 cells, the relative protein expression of VASH1 (0.751±0.035) was significantly higher in the pReceiver-M61VASH1 group, when compared with the level in the blank control (0.104±0.007) and pReceiver‐M61 group (0.102±0.024) (P
Summary
Renal cell carcinoma (RCC) is the most common neoplasm of the kidney in adults accounting for ~2-3% of all adult malignancies and 80-90% of primary malignant renal tumors [1,2]. Surgical resection is considered the first choice for treating RCC when possible and multiple treatments can be used together. It is important to develop novel tumor markers that have higher sensitivity and reliability and effective therapeutic methods for treating RCC. Tumor angiogenesis has been indicated to be a promising target for developing effective treatments for cancer patients. Among the pro-angiogenic factors, vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF) and hypoxia-inducible factor (HIF) families have been demonstrated to play important roles in mediating tumor angiogenesis, and are associated with tumor progression, invasion, metastasis and poor survival of patients with RCC [4,5,6,7]. The role of angiogenic inhibitors in RCC development is poorly understood
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