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在乳腺癌中 B7-H3 的表达与通过基因沉默上调 VEGF

 

Authors Sun J, Guo YD, Li XN, Zhang YQ, Gu L, Wu PP, Bai GH, Xiao Y

Published Date October 2014 Volume 2014:7 Pages 1979—1986

DOI http://dx.doi.org/10.2147/OTT.S63424

Received 3 March 2014, Accepted 26 June 2014, Published 29 October 2014

Abstract: B7-H3, a novel member of the B7 family, was previously known as a regulatory ligand regulating T-cell-mediated immune response, and in recent years it was found to take a significant role in various cancers. In some tumor types, high expression of B7-H3 had been linked to a poor prognosis, whereas in other cancers the opposite effect had been observed. The precise role of B7-H3 in tumor immunity is unclear, and further investigations are needed. In the present study, we studied the expression of B7-H3 in the pathologic specimens of 221 patients treated for breast cancer by immunohistochemistry. Strong B7-H3 expression was found in cancer tissues from 80.55% patients, and B7-H3 expression had a negative relation with vascular endothelial growth factor (VEGF) expression, microvascular density for CD34, and tumor size. Furthermore, through lipopolysaccharide-mediated delivery of stable short hairpin ribonucleic acid we observed that silencing of B7-H3 could increase the transcription and secreting of VEGF in breast cancer cell line MCF-7. In summary, the present study demonstrated that B7-H3 suppressed tumor growth through inhibiting VEGF expression. These results increased knowledge of the nonimmunological role of B7-H3 protein and provided novel insights into great biological functions and a putative therapeutic target in breast cancer.
Keywords: breast cancer, B7-H3, vascular endothelial growth factor






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