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利用基因转移技术，将新霉素抗性质粒ＰＳＶ２ｎｅｏ转入正常小鼠脾细胞，然后用ＰＥＧ促融，使其与具高转移力人肺巨细胞癌细胞系ＰＬＡ８０ｌ－Ｄ９５细胞融合，经Ｇ４１８筛选后获得１个无转移力克隆细胞系ＰＭＳ－２。染色体分析和以新霉素抗性基因为探针的ＤＮＡ－ＤＮＡ斑点杂交均证实，ＰＭＳ－２为杂种细胞克隆。裸鼠接种亲代肿瘤细胞３×１０６个细胞／只可发生明显的肺及淋巴结等脏器转移，接种ＰＭＳ－２７×１０６个细胞／只后仅能形成有完整包膜的肿瘤结节，无转移灶产生。此外，细胞的一般特性、生长速度、３Ｈ－ＴｄＲ参入率等也有明显的改变。提示正常小鼠脾细胞与肿瘤细胞融合后表现出的肿瘤转移能力抑制，可能由肿瘤转移抑制基因控制或其他水平干预所致。
Using gene transfer technology, the neomycin-resistant plasmid PSV2neo was transferred into normal mouse spleen cells, and then fused with PEG to enable fusion with PLA801-D95 cells with high metastasis capacity of human giant cell lung cancer cell line and screened by G418. Afterwards, a clone-free clone cell line PMS-2 was obtained. Chromosomal analysis and DNA-DNA dot blotting probed with a neomycin resistance gene all confirmed that PMS-2 is a hybrid cell clone. The nude mice were inoculated with 3×10 6 cells of the parental tumor cells and only obvious metastasis of lungs and lymph nodes could occur. PMS-27×10 6 cells inoculated could only form tumor tumor nodules with intact capsules. Foci production. In addition, the general characteristics of cells, growth rate, 3H-TdR participation rate, etc. also have significant changes. It is suggested that the inhibition of tumor metastasis demonstrated by fusion of normal mouse splenocytes with tumor cells may be caused by tumor metastasis suppressor genes or other levels of intervention.