Esko J D, Rostand K S, Weinke J L
Department of Biochemistry, School of Medicine, University of Alabama, Birmingham 35294.
Science. 1988 Aug 26;241(4869):1092-6. doi: 10.1126/science.3137658.
The role proteoglycans play in tumor formation was examined by measuring the tumorigenicity of proteoglycan-deficient Chinese hamster ovary cell mutants in nude mice. When 10(7) cells were injected subcutaneously, mutants with less than about 15% of the wild-type level of proteoglycan synthesis did not produce tumors. Mutants defective in the synthesis of heparan sulfate proteoglycans also did not form tumors, whereas mutants with altered chondroitin sulfate proteoglycans were tumorigenic. Tumors arose from mixtures of wild-type and nontumorigenic mutant cells and contained both cell types, suggesting that wild-type cell proteoglycans enabled mutant cells to survive. The failure of heparan sulfate-deficient mutants to form tumors depended on the ability of the host to mount a B cell-mediated immune reaction.
通过测量蛋白聚糖缺陷型中国仓鼠卵巢细胞突变体在裸鼠中的致瘤性，研究了蛋白聚糖在肿瘤形成中的作用。当皮下注射10⁷个细胞时，蛋白聚糖合成水平低于野生型水平约15%的突变体不会产生肿瘤。硫酸乙酰肝素蛋白聚糖合成缺陷的突变体也不会形成肿瘤，而硫酸软骨素蛋白聚糖发生改变的突变体具有致瘤性。肿瘤由野生型和非致瘤性突变体细胞的混合物产生，且包含这两种细胞类型，这表明野生型细胞蛋白聚糖能使突变体细胞存活。硫酸乙酰肝素缺陷型突变体无法形成肿瘤取决于宿主产生B细胞介导的免疫反应的能力。
