基于CYP19探讨雷公藤甲素抗ER(+)人乳腺癌MCF-7细胞作用机理

刘敏; 张露蓉; 梁国强; 简暾玉; 张晓迪

基于CYP19探讨雷公藤甲素抗ER(+)人乳腺癌MCF-7细胞作用机理

1.
南京中医药大学附属苏州市中医医院，江苏苏州 215009
2.
江苏省植物研究所，江苏南京 210014

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出版历程
- 收稿日期: 2017-01-05
- 修回日期: 2017-06-02
- 刊出日期: 2017-07-10

Study on Antiblastic Effect Mechanism of ER(+) Human Breast Cancer MCF-7 Cells by Triptolide Based on CYP19

1.
Affiliated Suzhou Hospital of TCM to Nanjing University of Chinese Medicine, Suzhou, 215009, China
2.
Jiangsu Province Institute of Botany, Nanjing, 210014, China

摘要

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。
- CYP19 /
- 雷公藤甲素 /
- 人乳腺癌MCF-7细胞 /
- 转染
Abstract: 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 decreased.Phosphorylation of JNK，p38 and ERK was inhibited too. CONCLUSION Triptolide inhibit MCF-7 cells not only via inhibition aromatase， but also blocking Ras-Raf-MAPK-ERK enzyme.
- CYP19 /
- triptolide /
- human breast cancer MCF-7 Cells /
- transfaction

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