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美《科学》第205卷(1979年)第691页报道:浓度为每毫升0.08微克的蛋白合成抑制剂放线菌酮能使基尔斯坦氏鼠肉瘤病毒(Ki-MSV)或N-甲基-N~1-氮-N-亚硝基胍(MNNG)转化的人骨肉瘤细胞在24～48小时内引起扁平形态及低饱和密度。去除蛋白合成抑制剂使二种转化的细胞逆转为转化的表现型。细胞表面抗原与二种转化的人细胞提取物诱发的抗血清交叉反应后的表现,决定于培养基中存在放线菌酮与否。结果表明,在病毒或化学转化的人细胞中,需要蛋白合成来维持其转化状态。
US Science, Vol. 205 (1979), p. 691 reports: The protein synthesis inhibitor cycloheximide at a concentration of 0.08 μg/ml can cause Kierstan’s murine sarcoma virus (Ki-MSV) or N-methyl -N~l-N-N-nitrosoguanidine (MNNG) transformed human osteosarcoma cells induce flat morphology and low saturation density within 24-48 hours. Removal of the protein synthesis inhibitor reverses the two transformed cells to the transformed phenotype. The performance of cell surface antigens after cross-reactivity with the antiserum induced by the two transformed human cell extracts is determined by the presence or absence of cycloheximide in the culture medium. The results show that in viral or chemically transformed human cells, protein synthesis is required to maintain their transformed state.