Wolf D A, Kohlhuber F, Schulz P, Fittler F, Eick D
Institut für Physiologische Chemie, Universität München, Germany.
Br J Cancer. 1992 Mar;65(3):376-82. doi: 10.1038/bjc.1992.76.
The mechanism of down-regulation of c-myc RNA associated with androgen-induced suppression of the transformed phenotype in the human prostate carcinoma cell line LNCaP was investigated. The synthetic androgen mibolerone (7 alpha-17 alpha-Dimethyl-19-nortestosterone) reversibly inhibits the proliferation of LNCaP cells and, from 12-72 h after hormone addition reduces the level of c-myc transcripts to a few per cent of controls. P1, P2, and P0 c-myc transcripts decline at the same rate, whereas P3 transcripts are much less hormone sensitive. Nuclear run-on analysis revealed that c-myc is down-regulated at the level of transcription initiation in LNCaP cells. The level of c-myc transcripts prevailing in untreated control cells can be restored in androgen-induced cells by excess antiandrogen, indicating the involvement of the androgen receptor in c-myc down-regulation.
研究了与雄激素诱导的人前列腺癌细胞系LNCaP中转化表型抑制相关的c-myc RNA下调机制。合成雄激素米勃龙（7α-17α-二甲基-19-去甲睾酮）可逆性抑制LNCaP细胞的增殖，并且在添加激素后12至72小时，将c-myc转录本水平降低至对照的百分之几。P1、P2和P0 c-myc转录本以相同速率下降，而P3转录本对激素的敏感性要低得多。核转录分析显示，LNCaP细胞中c-myc在转录起始水平被下调。通过过量抗雄激素可使雄激素诱导细胞中未处理对照细胞中占主导的c-myc转录本水平恢复，这表明雄激素受体参与了c-myc的下调。
