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

文献类型： 外文期刊

第一作者： Zhang Quan

作者： Zhang Quan;Zhai Guo Qin;Xue Zheng Feng;Xu Xiang Ming;Yuan Wei Feng;Zhu Hong Fei;Zhu Shan Yuan;Xu Xiang Ming

作者机构：

关键词： HVJ-E;Dendritic cell;Melanoma;beta-catenin

期刊名称：BIOMEDICAL AND ENVIRONMENTAL SCIENCES （ 影响因子：3.118； 五年影响因子：3.219 ）

ISSN： 0895-3988

年卷期： 2012 年 25 卷 5 期

页码：

收录情况： SCI

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 beta-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 beta-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 beta-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.

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