Eukaryotic translation initiation factors 3i (eIF3i) is a proto-oncogene that is overexpressed in various tumors, reducing its expression by eIF3i shRNA is a promising strategy to inhibit tumor growth or metastasis. Tumor cell is the target of eIF3i shRNA so that tumor-site accumulation could be important for fulfilling its therapeutic effect. Thus, the iRGD modified liposome (R-LP) was rationally synthesized to enhance the antitumor effect by active targeted delivery of eIF3i shRNA to B16F10 melanoma cells. R-LP encapsulating eIF3i shRNA gene (R-LP/sheIF3i) were prepared by a film dispersion method. The transfection experiment proves that R-LP could effectively transfect B16F10 cells. R-LP/sheIF3i notably restrained the migration, invasion, and adhesion of melanoma cells in vitro. In a mouse model of lung metastasis, R-LP/sheIF3i administered by intravenous injection suppressed pulmonary metastasis of melanoma by dramatically downregulated eIF3i expression and subsequently inhibiting tumor neovascularization and tumor cells proliferation in vivo. Our results provide a basis for tumor cells targeting strategies to reduce the expression of eIF3i by RNAi in the treatment of tumor metastasis.

中文翻译：

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eIF3i shRNA脂质体抑制黑色素瘤肺癌转移的癌症靶向基因治疗。

真核翻译起始因子3i（eIF3i）是一种原癌基因，在多种肿瘤中均过表达，通过eIF3i shRNA降低其表达是抑制肿瘤生长或转移的一种有前途的策略。肿瘤细胞是eIF3i shRNA的靶标，因此肿瘤部位的积累对于实现其治疗效果可能很重要。因此，通过将eIF3i shRNA主动靶向递送至B16F10黑色素瘤细胞，合理合成了iRGD修饰的脂质体（R-LP）以增强抗肿瘤作用。通过膜分散法制备了包裹eIF3i shRNA基因的R-LP（R-LP / sheIF3i）。转染实验证明R-LP可以有效转染B16F10细胞。R-LP / sheIF3i在体外显着抑制了黑色素瘤细胞的迁移，侵袭和粘附。在小鼠的肺转移模型中，静脉注射R-LP / sheIF3i通过显着下调eIF3i表达来抑制黑色素瘤的肺转移，并随后抑制体内肿瘤新血管形成和肿瘤细胞增殖。我们的结果为肿瘤细胞靶向策略以减少RNAi在肿瘤转移治疗中减少eIF3i的表达提供了基础。