摘要
目的基于CYP19基因阐明雷公藤甲素抗ER(+)人乳腺癌细胞的作用机制。方法雷公藤甲素组与来曲唑组相对照,采用MTT法观察雷公藤甲素对MCF-7细胞增殖的影响;采用Western blot观察其对芳香化酶的影响;采用RT-PCR观察其对CYP19基因的影响;采用瞬时转染形成高表达及低表达CYP19基因的MCF-7细胞,并用Western blot的方法观察雷公藤甲素对转染细胞CYP19以及其下游通路相关基因JNK、P38和ERK的影响。结果雷公藤甲素能明显抑制MCF-7细胞增殖(P<0.01),其抑制作用随着浓度增高和时间的延长而增强,能抑制芳香化酶及CYP19基因的表达,并能明显下调低表达CYP19-MCF-7细胞的CYP19表达,及抑制JNK、p-38和ERK的磷酸化。结论雷公藤甲素抗MCF-7细胞的作用机制之一,是通过抑制芳香化酶起作用,并引起下游Ras-Raf-MAPK-ERK激酶系统通路受抑制。
OBJECTIVE To investigate the mechanisms of Triptolide in ER（＋） human breast cancer MCF-7 cells from CYP19. METHODS The inhibition of the MCF-7 cells influenced by Triptolide and Letrozole was analyzed respectively by MTT assays. The aromatase levels were measured by Western blot. The CYP19 gene was observed by RT-PCR. The MCF-7 cells of high and low expression CYP19 gene were transfacted. It＇s CYP-19 and downstream channel gene JNK, p-38 and ERK were observed by Western blot. RESULTS Triptolide displayed a dose- and time-dependent inhibition of the MCF-7 cells. It inhibited the aromatase and CYP19. The expression of CYP19 in MCF-7 cells of low expression CYP19 was significantly de- creased. Phosphorylation of JNK, p38 and ERK was inhibited too. CONCLUSION Triptolide inhibit MCF-7 cells not only via inhibition aromatase, but also blockinu Ras-Raf-MAPK-ERK enzyme.
作者
刘敏
张露蓉
梁国强
简暾玉
张晓迪
LIU Min ZHANG Lu-rong LIANG Guo-qiang JIAN Dun-yu ZHANG Xiao-di(Affiliated Suzhou Hospital of TCM to Nanjing University of Chinese Medicine, Suzhou, 215009,China Jiangsu Province Institute of Botany, Nanjing, 210014,China)
出处
《南京中医药大学学报》
CAS
CSCD
北大核心
2017年第4期391-394,共4页
Journal of Nanjing University of Traditional Chinese Medicine
基金
江苏省中医药局科技项目(LZ13149)
苏州市科技局科技项目(SYS201572)
