類皮質糖荷爾蒙對 c-jun 基因表現之影響

Abstract

致癌基因jun在1987年被發現於禽類肉瘤病毒 (avian sarcoma virus 17)．目前已知其產物可與另一致癌基因fos之產物形成異質雙體（heterodimer),結合於AP-1位置上，遂行轉錄活化的作用．由於c-jun 的基因表現受到許多生長因數的影響（例如表皮生長因數，神經生長因數等等），我們預期其亦可接受一些荷爾蒙的調控，結果發現在加入類皮質糖荷爾蒙後4-12小時間產生約2倍的抑制效果，且此種抑制並不受到轉譯抑制劑的影響，為一原級反應．此種抑制的產生可能由於類皮質糖荷爾蒙受體與AP-1相互競爭結合位的結果，經由CAT檢定，發現該受體在AP-1位置附近有一弱結合位，此結果初步證明瞭這個假設．

The Jun oncogene has been identified in avian sarcoma virus 17 in 1987. The products of jun and fos form a heterodimer which can bind to AP-1 site and function as a transcriptional activator. Expression of c-jun proto-oncogene is generally regulated by various growth factors (e.g. epidermal growth factor, nerve growth factor). The first result of our experiments shows that after the treatment of glucocorticoid hormone, a twofold repression of transcriptional activity of c-jun can be observed within a 4-12 hours period. Further experiments prove such repression as a primarily response since it is not influenced by the presence of cycloheximide--a translation inhibitor. The repression may be due to a competitive binding between glucocorticoid receptor and Jun—Fos complex. This assumption is primarily proved by CAT assay which indicates a weak binding of this hormone receptor surrouding AP-1 site.