Trojan J, Johnson T R, Rudin S D, Ilan J, Tykocinski M L, Ilan J
INSERM, Paris.
Science. 1993 Jan 1;259(5091):94-7. doi: 10.1126/science.8418502.
Rat C6 glioma cells express insulin-like growth factor I (IGF-I) and form rapidly growing tumors in syngeneic animals. When transfected with an episome-based vector encoding antisense IGF-I complementary DNA, these cells lost tumorigenicity. Subcutaneous injection of IGF-I antisense-transfected C6 cells into rats prevented formation of both subcutaneous tumors and brain tumors induced by nontransfected C6 cells. The antisense-transfected cells also caused regression of established brain glioblastomas when injected at a point distal to the tumor. These antitumor effects result from a glioma-specific immune response involving CD8+ lymphocytes. Antisense blocking of IGF-I expression may reverse a phenotype that allows C6 glioma cells to evade the immune system.
大鼠C6胶质瘤细胞表达胰岛素样生长因子I（IGF-I），并在同基因动物中形成快速生长的肿瘤。当用编码反义IGF-I互补DNA的附加型载体转染时，这些细胞失去了致瘤性。将反义IGF-I转染的C6细胞皮下注射到大鼠体内，可阻止未转染的C6细胞诱导形成皮下肿瘤和脑肿瘤。当在肿瘤远端的一点注射时，反义转染的细胞还可使已形成的脑胶质母细胞瘤消退。这些抗肿瘤作用源于涉及CD8+淋巴细胞的胶质瘤特异性免疫反应。对IGF-I表达的反义阻断可能会逆转使C6胶质瘤细胞逃避免疫系统的表型。
