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Archive > Volume 20 Issue 3 > 2013,20(3):266-271. DOI:10.3872/j.issn.1007-385X.2013.03.002 Prev Next
Prompt Report
expression vector and its therapeutic effects on breast cancer D2F2 cell xenografts in mice
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Abstract:
Objective:To explore the inhibitory effect of mouse phosphatase of regenerating liver-3 (mPRL-3)-targeted DNA vaccine on the growth of mouse breast cancer D2F2 cells in vivo. Methods: The eukaryotic expression vector pVAX1-mPRL-3 targeting mPRL-3 was constructed and transfected into quail fibroblasts QM7 cells. The mPRL-3 protein expression in QM7 cells was detected by Western blotting. D2F2 mouse breast cancer cells were infected with recombinant lentivirus (Lv-mPRL-3) or control vector (Lv-Ctrl) to generate cells expressing mPRL-3 (mPRL-3-D2F2) or control cells (NC-D2F2), and the expression of mPRL-3 protein in mouse breast cancer D2F2 cells was analyzed by Western blotting. The mPRL-3-D2F2 and NC-D2F2 cells were respectively inoculated into BALB/c mice’s left mammary fad pat, then the BALB/c mice were immunized with pVAX1-mPRL-3 DNA vaccine (mPRL-3-D2F2/pVAX1-mPRL-3) by gene gun, and mPRL-3-D2F2/pVAX1-Ctrl and NC-D2F2/pVAX1-mPRL-3 were set as controls. The volume of tumor and the survival time of mice were monitored. Results: The eukaryotic expression vector pVAX1-mPRL-3 was identified by enzymatic digestion and DNA sequencing and the expression of mPRL-3 protein in QM7 cells was also confirmed. Western blotting assay results showed that the over-expression of mPRL-3 protein was detected in mPRL-3-D2F2, but not in NC-D2F2 cells. The tumor volume of the tumor-bearing mice immunized with pVAX1-mPRL-3 vaccine was significantly lower than that of the control group (\[835.3±509.8\] vs \[1543.0±578.4\] mm3, P<001\]. The pVAX1-mPRL-3 vaccination could significantly prolong the survival time of the tumor bearing mice (median survival time: 55.5 vs 38 d, P<005). Conclusion: PRL-3 -targeted vaccination mediated by gene gun can inhibit the growth of mouse breast cancer D2F2 cell xenografts expressing mPRL-3, which could be a potential therapy strategy for PRL-3 positive tumor.
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Project Supported:
Project supported by the National Key Basic Research Development Program (973 Program) of China (No. 2009CB521805)
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