DOWN-MODULATION OF AN ONCOGENE PROTEIN PRODUCT AND REVERSION OF THE TRANSFORMED PHENOTYPE BY MONOCLONAL-ANTIBODIES
DOWN-MODULATION OF AN ONCOGENE PROTEIN PRODUCT AND REVERSION OF THE TRANSFORMED PHENOTYPE BY MONOCLONAL-ANTIBODIES
复制标题
DOI：
10.1016/s0092-8674(85)80050-7
复制
发表时间：
1985-01-01
期刊：
影响因子：
64.5
通讯作者：
GREENE, MI
中科院分区：
文献类型：
--
作者：
DREBIN, JA;LINK, VC;GREENE, MI
将新致癌基因转化的NIH 3T3细胞暴露于与新基因产物p185反应的单克隆抗体中，会导致细胞表面和细胞总p185的快速可逆损失。虽然没有直接的细胞毒性，单克隆抗p185抗体处理导致新转化的NIH 3T3细胞恢复到非转化的表型，这是由锚定非依赖性生长确定的。不相关特异性的同型匹配对照抗体不影响新转化的NIH 3T3细胞在软琼脂中的p185水平或集落形成。ras癌基因转化的NIH 3T3细胞形成软琼脂集落不受抗p185抗体处理的影响。通过DNA转染检测到neu的乙基亚硝基源诱导的大鼠神经母细胞瘤细胞系的细胞在抗p185单克隆抗体的存在下也能抑制非锚定生长。显然p185是维持新癌基因诱导的转化所必需的。
Exposure of neu-oncogene-transformed NIH 3T3 cells to monoclonal antibodies reactive with the neu gene product, p185, results in the rapid and reversible loss of both cell-surface and total cellular p185. Although not directly cytotoxic, monoclonal anti-p185 antibody treatment causes neu-transformed NIH 3T3 cells to revert to a nontransformed phenotype, as determined by anchorage-independent growth. Isotype matched control antibodies of an unrelated specificity do not affect p185 levels or colony formation in soft agar by neu-transformed NIH 3T3 cells. Soft agar colony formation by NIH 3T3 cells transoformed by ras oncogenes is not affected by anti-p185 antibody treatment. Anchorage-independent growth of cells from the ethylnitrosourea-induced rat neuroblastoma line in which neu was originally detected by DNA transfection is also inhibited in the presence of anti-p185 monoclonal antibodies. Evidently p185 is required to maintain transformation induced by the neu oncogene.