Zuo Anjun, Zhao Peng, Zheng Yu, Hua Hui, Wang Xingang
Department of General Surgery, The Affiliated Hospital of Qingdao University, Qingdao 266000, China.
Department of Pathology, The Affiliated Hospital of Qingdao University, Qingdao 266000, China.
Biol Chem. 2019 Mar 26;400(8):1069-1078. doi: 10.1515/hsz-2018-0469. Print 2019 Jul 26.
Breast cancer is the most commonly diagnosed cancer in women worldwide. Tripterine is an important active component isolated from Hook F. This study investigated the effects of tripterine on breast cancer cell proliferation, migration, invasion and apoptosis, as well as microRNA-15a (miR-15a) expression. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to measure the expression of miR-15a. Cell transfection was conducted to change the expression of miR-15a. Viability, proliferation, migration, invasion and apoptosis of MDA-MB-231 cells were assessed using the cell counting kit-8 (CCK-8) assay, BrdU incorporation assay, Annexin V-FITC/PI apoptosis detection kit and two-chamber Transwell assay, respectively. Expression of key factors involving in cell proliferation, migration, invasion and apoptosis, as well as the PI3K/AKT and JNK pathways, were evaluated using Western blotting. We found that tripterine inhibited MDA-MB-231 cell viability, proliferation, migration and invasion, but induced cell apoptosis. Moreover, tripterine up-regulated the expression of miR-15a in a concentration-dependent manner and miR-15a participated in the effects of tripterine on MDA-MB-231 cell proliferation, migration, invasion and apoptosis. In addition, tripterine inactivated PI3K/AKT and JNK pathways in MDA-MB-231 cells by up-regulating miR-15a. In conclusion, tripterine inhibited proliferation, migration and invasion of breast cancer MDA-MB-231 cells by up-regulating miR-15a and inactivating PI3K/AKT and JNK pathways.
乳腺癌是全球女性中最常被诊断出的癌症。雷公藤红素是从雷公藤中分离出的一种重要活性成分。本研究调查了雷公藤红素对乳腺癌细胞增殖、迁移、侵袭和凋亡的影响，以及对微小RNA-15a（miR-15a）表达的影响。采用定量逆转录-聚合酶链反应（qRT-PCR）检测miR-15a的表达。通过细胞转染来改变miR-15a的表达。分别使用细胞计数试剂盒-8（CCK-8）检测法、BrdU掺入检测法、Annexin V-FITC/PI凋亡检测试剂盒和双室Transwell检测法评估MDA-MB-231细胞的活力、增殖、迁移、侵袭和凋亡。使用蛋白质免疫印迹法评估参与细胞增殖、迁移、侵袭和凋亡的关键因子以及PI3K/AKT和JNK信号通路的表达。我们发现雷公藤红素抑制MDA-MB-231细胞的活力、增殖、迁移和侵袭，但诱导细胞凋亡。此外，雷公藤红素以浓度依赖的方式上调miR-15a的表达，且miR-15a参与了雷公藤红素对MDA-MB-231细胞增殖、迁移、侵袭和凋亡的影响。此外，雷公藤红素通过上调miR-15a使MDA-MB-231细胞中的PI3K/AKT和JNK信号通路失活。总之，雷公藤红素通过上调miR-15a并使PI3K/AKT和JNK信号通路失活，抑制乳腺癌MDA-MB-231细胞的增殖、迁移和侵袭。
