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Canstatin inhibits growth, metastasis and angiogenesis of transplanted Lewis lung cancer in mice
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Abstract:
Objective : To investigate the effect of canstatin on growth, metastasis and angiogenesis of transplanted Lewis lung cancer in mice. Methods: The recombinant pCMV-Script/canstatin vector or the empty vector was transfected into A549 cells by electroporation, and the positive clones were screened with G418. The expressions of canstatin mRNA and protein in transfected A549 cells were examined by RT-PCR and Western blotting, respectively. Furthermore, transplanted Lewis lung cancer mouse model was established, and therapeutic effect of supernatant of pCMV-Script/canstatin transfected A549 cells on transplanted Lewis lung cancer was observed. Microvessel density of transplanted tumors in different therapy groups was observed by immunohistochemistry. Results: Positive clones of A549 cells transfected with pCMV-Script/canstatin were successfully obtained by G418 screening, and could effectively express canstatin mRNA and protein. The tumor size of the pCMV-Script/canstatin group (1.47±0.21 cm3) was significantly smaller than that in the pCMV-Scrip group (2.43±0.15 cm3) and NS group (2.53±0.18 cm3) (P<0.01). The number of pulmonary metastatic nodes was 3.00±1.00, 7.80±1.48 and 7.60±2.41 respectively for pCMV-Script/canstatin, pCMV-Script and NS groups, so pCMV-Script/canstatin significantly inhibited metastasis of tumors (P<0.01). The amount of microvessel count (MVC) in pCMV-Script/canstatin group was markedly decreased compared to that of pCMV-Script and NS groups (P<0.01). Conclusion: The pCMV-Script/canstatin mediates expression of canstatin in A549 cells. Canstatin in A549 supernantant has a strong inhibitory effect on growth, metastasis and angiogenesis of Lewis lung carcinoma.
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