Cossu G, Pacifici M, Adamo S, Bouché M, Molinaro M
Differentiation. 1982;21(1):62-5. doi: 10.1111/j.1432-0436.1982.tb01197.x.
The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) dramatically modifies the differentiative program of myotubes, developed in culture from chick embryo skeletal myogenic cells. In fact TPA selectively decreases the expression of differentiative parameters with a lag of 8-10 h from its administration to the cultures. We have tested whether the reported effect of TPA depends on the synthesis of specific products during the lag phase of TPA action. The data presented indicate that inhibition of protein synthesis by the use of cycloheximide prevents the appearance of TPA induced inhibition of the expression of differentiative products, such as creatine phosphokinase (CPK) activity and acetylcholine receptors (AChR). Following removal of cycloheximide and reinitiation of normal protein synthesis, the TPA induced inhibitory effect on CPK and AChR appears after a delay of about the same length as the time lag of TPA action. Our results indicate that inhibition of protein synthesis during the lag phase of TPA action prevents the effect of this tumor promoter on myotube differentiative parameters, and suggest that the expression of differentiative traits in cultured myotubes is affected by TPA via a regulatory step implying protein synthesis.
肿瘤促进剂十四酰佛波醇乙酯（TPA）可显著改变鸡胚骨骼肌成肌细胞在培养中发育形成的肌管的分化程序。事实上，TPA从加入培养物开始，经过8 - 10小时的延迟后，选择性地降低了分化参数的表达。我们测试了TPA的上述作用是否取决于TPA作用延迟期内特定产物的合成。所呈现的数据表明，使用放线菌酮抑制蛋白质合成可阻止TPA诱导的对分化产物表达的抑制，如肌酸磷酸激酶（CPK）活性和乙酰胆碱受体（AChR）。去除放线菌酮并重新开始正常蛋白质合成后，TPA对CPK和AChR的诱导抑制作用在延迟约与TPA作用延迟时间相同的时长后出现。我们的结果表明，在TPA作用延迟期抑制蛋白质合成可阻止这种肿瘤促进剂对肌管分化参数的影响，并提示培养的肌管中分化特征的表达受TPA影响，是通过一个涉及蛋白质合成的调控步骤实现的。
