Suppression of tumorigenicity in hybrids of normal and oncogene-transformed CHEF cells.
Suppression of tumorigenicity in hybrids of normal and oncogene-transformed CHEF cells.
复制标题
抑制正常和癌基因转化的 CHEF 细胞的杂交体的致瘤性。
DOI：
10.1073/pnas.82.7.2062
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发表时间：
1985
影响因子：
11.1
通讯作者：
Sager,R
中科院分区：
文献类型：
--
作者：
Craig,RW;Sager,R
进行体细胞杂交实验以确定正常细胞是否有能力抑制特定癌基因的转化作用。以未转化的中国仓鼠胚成纤维细胞系（CHEF/18-dm2）为正常亲本，以携带人突变型c-Ha-ras （EJ）致癌基因的CHEF/18转染物为致瘤亲本。选择的杂种（L318细胞系）检测EJ DNA的存在，c-Ha-ras基因的p21产物，以及细胞转化的各种指标。这些杂交种表现出与正常亲本相似的成纤维细胞形态，尽管它们含有EJ基因，其p21蛋白产物的表达水平与转化的亲本相当。它们的不依赖锚定生长能力降低（甲基纤维素的镀效率低于0.3-13%，而转化的亲本的镀效率高于90%），胸腺小鼠的肿瘤形成能力降低。这些发现表明，正常的CHEF/18细胞含有抑制基因，能够在激活的EJ癌基因存在下抑制转化表型的表达和肿瘤形成能力。
Somatic cell hybridization experiments were carried out to determine whether normal cells have the ability to suppress the transforming effects of a defined oncogene. A nontransformed Chinese hamster embryo fibroblast cell line (CHEF/18-dm2) was used as the normal parent, and a CHEF/18 transfectant carrying the human mutant c-Ha-ras (EJ) oncogene was used as the tumorigenic parent. Selected hybrids (L318 cell lines) were assayed for the presence of EJ DNA, for the p21 product of the c-Ha-ras gene, and for various indices of cell transformation. These hybrids exhibited a fibroblastic morphology similar to the normal parent, although they contained the EJ gene and expressed its p21 protein product at levels comparable with the transformed parent. They had a reduced capacity for anchorage-independent growth (plating efficiency in methylcellulose of less than 0.3-13%, as compared with greater than 90% for the transformed parent) and decreased tumor-forming ability in athymic mice. These findings show that normal CHEF/18 cells contain suppressor genes capable of inhibiting expression of the transformed phenotype, and tumor-forming ability, in the presence of an activated EJ oncogene.