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Thrombospondin 1 Triggers Osteosarcoma Cell Metastasis and Tumor Angiogenesis

Yue Kui Jian1, Huan Ye Zhu1, Xing Lin Wu, Bo Li

Affiliated People’s Hospital of Guizhou Medical University, Guiyang, P.R. China

Oncology Research 2019, 27(2), 211-218. https://doi.org/10.3727/096504018X15208993118389

Abstract

Osteosarcomas, especially those with metastatic or unresectable disease, have limited treatment options. The antitumor effects of pharmacologic inhibitors of angiogenesis in osteosarcomas are hampered in patients by the rapid development of tumor resistance, notably through increased invasiveness and accelerated metastasis. Here we demonstrated that thrombospondin 1 (TSP-1) is a potent inhibitor of the growth and metastasis of the osteosarcoma cell line MG-63. Moreover, we demonstrate that upregulation of TSP-1 facilitated expression of vasculostatin in MG-63 cells. In angiogenesis assays, overexpression of TSP-1 inhibited MG-63 cells and induced tube formation of human umbilical vein endothelial cells (HUVECs) in a CD36-dependent fashion. Finally, in xenografted tumors, we observed that TSP-1 overexpression inhibited angiogenesis and tumor growth. These results provided strong evidence for an important role of the TSP-1/CD36/vasculostatin signaling axis in mediating the antiangiogenic activity of osteosarcoma.

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APA Style
Jian, Y.K., Zhu, H.Y., Wu, X.L., Li, B. (2019). Thrombospondin 1 triggers osteosarcoma cell metastasis and tumor angiogenesis. Oncology Research, 27(2), 211-218. https://doi.org/10.3727/096504018X15208993118389
Vancouver Style
Jian YK, Zhu HY, Wu XL, Li B. Thrombospondin 1 triggers osteosarcoma cell metastasis and tumor angiogenesis. Oncol Res. 2019;27(2):211-218 https://doi.org/10.3727/096504018X15208993118389
IEEE Style
Y.K. Jian, H.Y. Zhu, X.L. Wu, and B. Li, “Thrombospondin 1 Triggers Osteosarcoma Cell Metastasis and Tumor Angiogenesis,” Oncol. Res., vol. 27, no. 2, pp. 211-218, 2019. https://doi.org/10.3727/096504018X15208993118389



cc Copyright © 2019 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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