Inactivated Sendai Virus Suppresses Murine Melanoma Growth by Inducing Host Immune Responses and Down-regulating β-catenin Expression

查看全文 作　　者：ZHANG [1]Quan;YUAN Wei [2]Feng;ZHAI Guo [1]Qin;XUE Zheng [1]Feng;ZHU Hong [2]Fei;XU Xiang [1,3]Ming

机构地区：[1]College of Veterinary Medicine,Yangzhou UniversRy,Yangzhou 225009,Jiangsu,China;[2]Institute of Animal Science and Veterinary Medicine,Chinese Academy of Agricultural Sciences,Beijing 100081,China;[3]Key Laboratory of Animal-used High-tech Biopharmaceutical of Jiangsu Province,Taizhou 225300,Jiangsu,China

出　　处：《Biomedical and Environmental Sciences》索引2012年第25卷第5期,共8页

基　　金：supported by a grant from the National High Technology Research and Development Program of China(2012AA101302);Natural Science Foundation of Jiangsu Province(BK2011049);Jiangsu'333'projects in Jiangsu province(BK201140032) 摘　　要：Objective This paper aims to investigate the anti-tumor mechanism of inactivated Sendai virus (Hemagglutinating virus of Japan envelope, HVJ-E) for murine melanoma (B16F10). Methods The murine dendritic cells (DCs) were treated with HVJ-E, and then the cytokines secreted from DCs and costimulation-related molecules on DCs were measured. Meanwhile, the expression of β-catenin in HVJ-E treated murine melanoma cells was detected. In addition, HVJ-E was intratumorally injected into the melanoma on C57BL/6 mice, and the immune cells, CTL response and tumor volume were analyzed. Results HVJ-E injected into B16F10 melanoma obviously inhibited the growth of the tumor and prolonged the survival time of the tumor-bearing mice. Profiles of cytokines secreted by dendritic cells (DCs) after HVJ-E stimulation showed that the number of cytokines released was significantly higher than that elicited by PBS (P<0.05). The co-stimulation-related molecules on DCs were comparable to those stimulated by LPS. Immunohistochemical examinations demonstrated the repression of β-catenin in B16F10 melanoma cells after HVJ-E treatment. Meanwhile, real-time reverse transcription PCR revealed that HVJ-E induced a remarkable infiltration of CD11c positive cells, chemokine ligand 10 (CXCL10) molecules, interleukin-2 (IL-2) molecule, CD4 + and CD8 + T cells into HVJ-E injected tumors. Furthermore, the mRNA expression level of β-catenin in the HVJ-E injected tumors was also down-regulated. In addition, B16F10-specific CTLs were induced significantly after HVJ-E was injected into the tumor-bearing mice. Conclusion This is the first report to show the effective inhibition of melanoma tumors by HVJ-E alone and the mechanism through which it induces antitumor immune responses and regulates important signal pathways for melanoma invasion. Therefore, HVJ-E shows its prospect as a novel therapeutic for melanoma therapy. 关键词：黑色素瘤荷瘤小鼠病毒诱导免疫反应灭活生长逆转录聚合酶链反应抗肿瘤机制

相关文献

参考文献（25）
引证文献（9）
耦合文献（0）

参考文献(25)

引证文献(9)

互联网出版许可证新出网证(渝)字10号全国400电话 - 免长途话费

Inactivated Sendai Virus Suppresses Murine Melanoma Growth by Inducing Host Immune Responses and Down-regulating β-catenin Expression

参考文献(25)

引证文献(9)

用户提示