Marciani D J, Lyons L B, Thompson E B
Cancer Res. 1976 Aug;36(8):2937-44.
Cell membranes from mouse L-cells (L-B82), rat hepatoma (HTC-H1), and three clones of their somatic cell hybrids (07, V4a, and V5) showing different degrees of density-dependent inhibition of growth were analyzed by polyacrylamide gel electrophoresis. The membrane polypeptides of the hybrid clones were all similar and all showed higher proportions of polypeptides with molecular weights of 56,000 and 45,000 than their parents of their normal counterparts. The major glycoprotein form cell hybrids appeared to be identical with that of rat liver or rat hepatoma cells and different from that of L-cells. One hybrid showed density-dependent inhibition growth; the other two, like both parents, did not. All produced tumors in nude mice, although tumor production by the hybrids was delayed. A large external protein (M.W. 240,000) iodinated by lactoperoxidase-catalyzed reaction was virtually missing in the parents but was present at high levels in all their hybrid clones. Thus, there was a lack of correlation between the presence of this protein, growth control in vitro, and tumorigenicity. Furthermore, no correlation was seen between agglutination of these cells by concanavalin A and tumorigenicity. The factors controlling these membrane properties thus are independent of density-dependent inhibition of growth and of those controlling the expression of cancer.
对来自小鼠L细胞（L - B82）、大鼠肝癌细胞（HTC - H1）及其三个体细胞杂交克隆（07、V4a和V5）的细胞膜进行了聚丙烯酰胺凝胶电泳分析，这些杂交克隆表现出不同程度的密度依赖性生长抑制。杂交克隆的膜多肽都相似，且与它们的亲本或正常对应物相比，分子量为56,000和45,000的多肽比例更高。杂交细胞的主要糖蛋白形式似乎与大鼠肝脏或大鼠肝癌细胞的相同，与L细胞的不同。一个杂交克隆表现出密度依赖性生长抑制；另外两个则像它们的亲本一样，没有表现出这种抑制。所有这些细胞在裸鼠中都能产生肿瘤，尽管杂交细胞产生肿瘤的时间有所延迟。一种由乳过氧化物酶催化反应碘化的大的外部蛋白（分子量240,000）在亲本细胞中几乎不存在，但在它们所有的杂交克隆中含量都很高。因此，这种蛋白的存在、体外生长控制和致瘤性之间缺乏相关性。此外，伴刀豆球蛋白A对这些细胞的凝集作用与致瘤性之间也没有相关性。因此，控制这些膜特性的因素独立于密度依赖性生长抑制以及控制癌症表达的因素。
