These authors equally contributed to this study.
HER2/neu expression correlates with vasculogenic mimicry in invasive breast carcinoma
Article first published online: 19 DEC 2012
© 2012 The Authors Journal of Cellular and Molecular Medicine Published by Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Journal of Cellular and Molecular Medicine
Volume 17, Issue 1, pages 116–122, January 2013
How to Cite
Liu, T., Sun, B., Zhao, X., Gu, Q., Dong, X., Yao, Z., Zhao, N., Chi, J., Liu, N., Sun, R. and Ma, Y. (2013), HER2/neu expression correlates with vasculogenic mimicry in invasive breast carcinoma. Journal of Cellular and Molecular Medicine, 17: 116–122. doi: 10.1111/j.1582-4934.2012.01653.x
- Issue published online: 29 JAN 2013
- Article first published online: 19 DEC 2012
- Manuscript Accepted: 8 OCT 2012
- Manuscript Received: 20 JUL 2012
- National Natural Science Foundation of China. Grant Number: 30830049
- International Cooperation Project of China–Sweden. Grant Number: 09ZCZDSF04400
- National Natural Science Foundation of China. Grant Number: 81172046
- National Natural Science Foundation of China. Grant Numbers: 81173091, 20111202110010
- Tianjin Natural Science Foundation. Grant Numbers: 12JCZDJC23600, 10JCZDJC20400
- Ministry of Science and Technology of China. Grant Number: 2009CB918903
- Ministry of Science and Technology of China. Grant Number: 2011CB933104
- Natural Science Foundation of Tianjin Education Commission. Grant Number: 20100106
- vasculogenic mimicry;
- breast cancer
Vasculogenic mimicry (VM) refers to the condition in which tumour cells mimic endothelial cells to form extracellular matrix-rich tubular channels. VM is more extensive in more aggressive tumours. The human epidermal growth factor receptor 2 (HER2) gene is amplified in 20–30% of human breast cancers and has been implicated in mediating aggressive tumour growth and metastasis. However, thus far, there have been no data on the role of HER2 in VM formation. Immunohistochemical and histochemical double-staining methods were performed to display VM in breast cancer specimens. Transfection in MCF7 cells was performed and clones were selected by G418. The three-dimensional Matrigel culture was used to evaluate VM formation in the breast cancer cell line. According to statistical analysis, VM was related to the presence of a positive nodal status and advanced clinical stage. The positive rate of VM increased with increased HER2 expression. In addition, cases with HER2 3+ expression showed significantly greater VM channel count than those in other cases. The exogenous HER2 overexpression in MCF-7 cells induced vessel-like VM structures on the Matrigel and increased the VM mediator vascular endothelial (VE) cadherin. Our data provide evidence for a clinically relevant association between HER2 and VM in human invasive breast cancer. HER2 overexpression possibly induces VM through the up-regulation of VE cadherin. Understanding the key molecular events may provide therapeutic intervention strategies for HER2+ breast cancer.