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Article

Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma

  • Authors:
    • Guangning Zhao
    • Ren Na
    • Liming Li
    • Huiyuan Xiao
    • Na Ding
    • Yan Sun
    • Ruifa Han
  • View Affiliations / Copyright

    Affiliations: Department of Urology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China, Department of Clinical Laboratory, Tianjin Children's Hospital, Tianjin 300074, P.R. China, Department of Urology, Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin 300211, P.R. China
  • Pages: 1021-1028
    |
    Published online on: June 22, 2017
       https://doi.org/10.3892/or.2017.5746
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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/G1 phase and promoted cell apoptosis of HUVECs and 786-0 cells. VASH1 overexpression effectively inhibited the subcutaneous growth of 786-0 tumors in vivo. Therefore, VASH1 is a potential molecular-targeted therapy for patients with RCC.
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Copy and paste a formatted citation
Spandidos Publications style
Zhao G, Na R, Li L, Xiao H, Ding N, Sun Y and Han R: Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma. Oncol Rep 38: 1021-1028, 2017.
APA
Zhao, G., Na, R., Li, L., Xiao, H., Ding, N., Sun, Y., & Han, R. (2017). Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma. Oncology Reports, 38, 1021-1028. https://doi.org/10.3892/or.2017.5746
MLA
Zhao, G., Na, R., Li, L., Xiao, H., Ding, N., Sun, Y., Han, R."Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma". Oncology Reports 38.2 (2017): 1021-1028.
Chicago
Zhao, G., Na, R., Li, L., Xiao, H., Ding, N., Sun, Y., Han, R."Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma". Oncology Reports 38, no. 2 (2017): 1021-1028. https://doi.org/10.3892/or.2017.5746
Copy and paste a formatted citation
x
Spandidos Publications style
Zhao G, Na R, Li L, Xiao H, Ding N, Sun Y and Han R: Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma. Oncol Rep 38: 1021-1028, 2017.
APA
Zhao, G., Na, R., Li, L., Xiao, H., Ding, N., Sun, Y., & Han, R. (2017). Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma. Oncology Reports, 38, 1021-1028. https://doi.org/10.3892/or.2017.5746
MLA
Zhao, G., Na, R., Li, L., Xiao, H., Ding, N., Sun, Y., Han, R."Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma". Oncology Reports 38.2 (2017): 1021-1028.
Chicago
Zhao, G., Na, R., Li, L., Xiao, H., Ding, N., Sun, Y., Han, R."Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma". Oncology Reports 38, no. 2 (2017): 1021-1028. https://doi.org/10.3892/or.2017.5746
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