NGcGM3/VSSP 疫苗通过抗 N-糖基化神经节苷脂过表达的转染 B16 小鼠黑色素瘤细胞的抗肿瘤保护作用。
Antitumor protection by NGcGM3/VSSP vaccine against transfected B16 mouse melanoma cells overexpressing N-glycolylated gangliosides.
机构信息
Laboratory of Molecular Oncology, Department of Science and Technology, Quilmes National University, R. Saenz Peña 352, Bernal B1876BXD Buenos Aires, Argentina.
出版信息
In Vivo. 2012 Jul-Aug;26(4):609-17.
BACKGROUND
Cancer vaccines are designed to modulate immunological responses against tumor cells through the presentation of tumor antigens.
MATERIALS AND METHODS
The mouse mRNA of the cytidine monophospho-N-acetylneuraminic acid hydroxylase (Cmah) gene, the enzyme that catalyzes the synthesis of N-glycolylneuraminic acid (NGc), was cloned and transfected into the B16 melanoma cell line. Transfected cells (B16-H) were characterized and used as an NGcGM3-positive primary tumor model for the evaluation of the therapeutic activity of the NGcGM3/VSSP vaccine.
RESULTS
The presence of NGcGM3 in B16-H cells promoted proliferation and adhesion in vitro, but resulted in reduced tumorigenicity in vivo. However, B16-H cells developed growing tumors in mice where NGcGM3/VSSP vaccination induced a therapeutic antitumor activity. NGcGM3/VSSP was ineffective in mice inoculated with parental B16 or B16-H cells that had lost NGcGM3 expression.
CONCLUSION
The presence of NGcGM3 in tumor cells is critical for the antitumor activity of NGcGM3/VSSP vaccine.
背景
癌症疫苗旨在通过呈现肿瘤抗原来调节针对肿瘤细胞的免疫反应。
材料和方法
克隆并转染小鼠胞苷单磷酸-N-乙酰神经氨酸羟化酶（Cmah）基因的 mRNA，该酶催化 N-羟乙酰神经氨酸（NGc）的合成。转染的细胞（B16-H）进行了表征，并用作 NGcGM3 阳性原发性肿瘤模型，用于评估 NGcGM3/VSSP 疫苗的治疗活性。
结果
B16-H 细胞中 NGcGM3 的存在促进了体外的增殖和黏附，但导致体内肿瘤生成能力降低。然而，在接种 NGcGM3/VSSP 的小鼠中，B16-H 细胞会发展成生长中的肿瘤，从而诱导出治疗性的抗肿瘤活性。NGcGM3/VSSP 在接种失去 NGcGM3 表达的亲本 B16 或 B16-H 细胞的小鼠中无效。
结论
肿瘤细胞中 NGcGM3 的存在对于 NGcGM3/VSSP 疫苗的抗肿瘤活性至关重要。
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