Inhibiting effects on invasion and metastasis of melanoma by CXCR4 gene silence in nude mice
10.3760/cma.j.issn.1671-0290.2012.02.016
- VernacularTitle:CXCR4基因沉默对小鼠黑素瘤的抑瘤效应及器官转移影响
- Author:
Baojin WU
;
Wenpeng LI
;
Hua JIANG
;
Jianming WU
;
Yingfan ZHANG
;
Wei DING
- Publication Type:Journal Article
- Keywords:
Melanoma;
Chemokin receptor CXCR4;
Gene silencing;
Tumor metastasis
- From:
Chinese Journal of Medical Aesthetics and Cosmetology
2012;18(2):136-139
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo study the inhibiting effects on the invasion and metastasis of melanoma by CXCR4 gene silence in nude mice.MethodsThe CXCR4 specific recombinant plasmid vector was constructed and transfected into the cultured MV3 cell line with lipofectamine.The models of subcutaneous melanoma in nude mice were established with MV3 cells.The nude mouse model of lung metastasis was established by injection of MV3 cells into the tail vein.The animals were sacrificed at 8weeks after the melanoma cells injection.CXCR4-shRNA plasmid vectors were discontinuously injected directly into the established tumor and vein.The changes of weight and size of the tumors and the mice body weight during the therapy were calculated respectively.Histological observation was performed to evaluate the presence and number of metastatic tumors.ResultsThe subcutaneous melanoma tumors in nude mice were established successfully.The growth of tumors in the CXCR4-shRNA injected nude mice was inhibitted obviously through tumor growth curve. There were significant differences between negative shRNA control nude mice and blank control nude mice (P<0.01).Melanoma cells with CXCR4 shRNA permanent transfection had a much lower lung and brain and liver metastatic potential in nude mice than control cells and mock control cells in vivo.ConclusionsCXCR4 gene silencing mediated by shRNA significantly suppresses the growth of MV3 cell in vitro.Silencing of CXCR4 mediated by shRNA can also effectively decrease the metastatic potential of lung and liver and brain.