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[Suppression of multiple myeloma tumor growth in vivo by transfection of platelet factor 4 or 17-70 cDNA].

作者信息

Yang Long-Jiang, Jiang Hua, Zou Jian-Feng, Hou Jian

机构信息

Department of Hematology, Changzheng Hospital, The Second Military Medical University, Shanghai 200003, China.

出版信息

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2010 Oct;18(5):1172-6.

Abstract

This study was purposed to investigate the effects of viral vector-mediated gene transfer of platelet factor 4 (PF4) or 17-70 cDNA on cell growth of multiple myeloma (MM) in vivo. Full length and p17-70 cDNA of PF4 were cloned into virapower system to transfect packing cell line 293 and produce lentiviral vectors. 3 multiple myeloma cell lines were transferred platelet factor 4 or 17-70 cDNA by lentiviral vectors. SCID-rab mice models of multiple myeloma were established by injecting U266 multiple myeloma cells selected. The human light chain proteins and VEGF in serums of mice were detected every 2 weeks. The volumes and vascular density of tumors as well as survival time of mice were observed. The results showed that the MM cells expressing foreign genes were identified and screened. There were significant difference of VEGF levels in the supernatants of MM cells between each groups (p<0.01). The SCID-rab models of U266 cells were established successfully. There were significant differences in light chain protein and VEGF in serums among three groups (p<0.01). The light chain protein and VEGF in mice serums of 17-70 cDNA groups were less than that of PF4 group (p<0.01). The light chain protein and VEGF in mice serums of PF4 group were less than that of control group (p<0.01). There were significant differences in the tumor volumes and the vascular density of tumor among 3 groups (p<0.05). The results also showed that there were significant differences of overall survival in 3 different groups of SCID-rab MM models. The overall survival in control group was shortest as compared with other groups (p<0.05). It is concluded that the cell growth of multiple myeloma is suppressed in vivo by transfection of platelet factor 4 or 17-70 cDNA and the overall survival of transfected mice will be prolonged.

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