Abstract
Abstract Vasostatin (VAS), a 180-amino acid fragment from the N-terminal domain of calreticulin, is a potent endogenous angiogenesis inhibitor, which can inhibit the growth of many kinds of experimental tumors. However, a recent report that vasostatin can enhance the malignant behavior of the neuroendocrine tumor reminds us to be cautious to develop it as an antitumor medicine. VA S cDNA was cloned into pAAV-2 expression vector; recombinant virus rAAV-VAS was generated by a three-plasmid, helper-free packaging method. MS1 mouse pancreatic endothelial cell and human colon tumor HCT-116 cell were infected with rAAV-VAS. Transgene expression was analyzed by Western blot analysis and cell proliferation was determined by MTT assay. The therapeutic potential of rAAV-VAS was evaluated in a subcutaneous HCT-116 xenograft mouse model. rAAV-VAS inhibited the proliferation of MS1, but not the HCT-116 cell. The HCT-116 cell, infected with rAAV-VAS, secreted VAS protein into the supernatant effectively. The intratumoral delivery of rAAV-VAS inhibited the xenograft growth and microvessel density in tumors significantly. The results show the effectiveness of rAAV-VAS as an angiogenesis inhibitor in suppressing tumor growth, validating the application of the rAAV-VAS gene therapy in treatment against colon cancer.
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