Anti-cancer activity of Annexin V in murine melanoma model by suppressing tumor angiogenesis
Metrics: PDF 1299 views | HTML 2632 views | ?
Xuerui Zhang1,2, Lina Huo1, Haibo Jin1, Yuheng Han1, Jie Wang1, Yanjun Zhang1, Xinghuan Lai1, Ziwei Le1, Jing Zhang1 and Zichun Hua1,2,3
1The State Key Laboratory of Pharmaceutical Biotechnology, School of Life Science, Nanjing University, Nanjing 210093, Jiangsu, China
2Changzhou High-Tech Research Institute of Nanjing University and Jiangsu Target Pharma Laboratories Inc., Changzhou 213164, Jiangsu, China
3The State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, Jiangsu, China
Jing Zhang, email: email@example.com
Zichun Hua, email: firstname.lastname@example.org
Keywords: Annexin V, apoptosis, necrosis, tumor angiogenesis
Received: November 17, 2016 Accepted: February 28, 2017 Published: March 29, 2017
Annexin V, a protein with high affinity to phosphatidylserine (PS) in a calcium dependent manner, has been widely used to probe apoptosis. Annexin V in inhibiting engulfment of apoptotic cells by macrophages had been reported to increase the immunogenicity of tumor cells undergoing apoptosis. However, far less is known about its multiple properties, especially in cancer therapies. Here we found that Annexin V had a good anti-tumor activity in murine melanomaxenograft model. Treatment with Annexin V showed significant reduction in tumor size and remarkable tumor necrosis areas. The serum level of VEGF was downregualted by Annexin V both in normal mice and mice bearing tumor, suggesting that its new role on impeding tumor angiogenesis. In Silico analysis using Oncomine database, we also found the negative correlation of AnnexinV and VEGF both in skin and melanoma. The decreased Annexin V expression shows linearity relation with the elevated VEGF expression. These data provided a possibility that Annexin V can be used as a novel angiogenesis inhibitor in tumor therapy.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.