Ripka J, Shin S, Stanley P
Mol Cell Biol. 1986 Apr;6(4):1268-75. doi: 10.1128/mcb.6.4.1268-1275.1986.
To investigate a role for surface carbohydrates in cellular malignancy, 15 different glycosylation-defective CHO cell mutants were examined for their tumorigenic and metastatic capacities after subcutaneous injection into nude mice. Most of the glycosylation mutants displayed similar or slightly decreased tumorigenicity compared with parental CHO cells. Neither parental CHO cells nor any of the mutants were observed to metastasize. However, independent isolates of one mutant type, Lec9, showed a dramatic reduction in tumor formation. The altered carbohydrates expressed at the surface of Lec9 cells appeared to be responsible for their loss of tumorigenicity, because revertants for lectin resistance were able to form tumors, and a double mutant (Lec9.Lec1) that expressed a Lec1 glycosylation phenotype also formed tumors. Finally, Lec9 cells were able to form tumors in gamma-irradiated nude mice, suggesting that recognition by an irradiation-sensitive host cell(s) was responsible for their reduced tumorigenicity in untreated nude mice.
为了研究表面碳水化合物在细胞恶性肿瘤中的作用,将15种不同的糖基化缺陷型CHO细胞突变体皮下注射到裸鼠体内后,检测它们的致瘤和转移能力。与亲本CHO细胞相比,大多数糖基化突变体表现出相似或略有降低的致瘤性。未观察到亲本CHO细胞或任何突变体发生转移。然而,一种突变类型Lec9的独立分离株显示肿瘤形成显著减少。Lec9细胞表面表达的碳水化合物改变似乎是其致瘤性丧失的原因,因为凝集素抗性回复株能够形成肿瘤,并且表达Lec1糖基化表型的双突变体(Lec9.Lec1)也能形成肿瘤。最后,Lec9细胞能够在经γ射线照射的裸鼠中形成肿瘤,这表明未处理的裸鼠中其致瘤性降低是由于对辐射敏感的宿主细胞的识别所致。