中药复方MAJ100对三阴性乳腺癌细胞的抑制与机制初探

Exploration of the inhibition effects and mechanisms of traditional Chinese medicine formula MAJ100 on triple-negative breast cancer cells

目的探究中药复方MAJ100对三阴性乳腺癌(TNBC)细胞的抑制作用,初步研究其机制。方法通过CCK-8以及细胞克隆形成能力测定细胞活力;借助流式细胞仪检测细胞的凋亡;采用Transwell细胞实验揭示MAJ100对肿瘤细胞迁移的影响;结合转录组测序结果探讨其作用机制。结果MAJ100以时间剂量依赖方式抑制MDA-MB-231细胞的活力,诱导肿瘤细胞凋亡,且抑制细胞增殖和迁移。MAJ100对TNBC的抑制可能与上调CDKN1A、下调CCNB1、CCNB2、CDK1等基因表达,抑制肿瘤细胞周期、影响P53信号通路有关。结论MAJ100可能通过多靶点、多途径抑制TNBCMDA-MB-231细胞的活性和迁移,并促进细胞凋亡。

OBJECTIVE To observe the effects of the traditional Chinese medicine formula MAJ100 on the inhibition of triple-negative breast cancer(TNBC)cells and to investigate its tentative mechanism.METHODS CCK-8 and clone formation assays were used to determine cell viability;flow cytometry was used to detect cell apoptosis;transwell cell assays were used to determine the effect of the formula on cell migration;finally,transcriptome sequencing data was required for a preliminary investigation of the mechanism.RESULTS MAJ100 could decrease the survival of MDA-MB-231 in a dose-dependent manner,promotes cancer cell apoptosis and inhibit cancer cell growth and migration.The suppression of MAJ100 for TNBC cells might be linked to the lower expressions of CCNB1,CCNB2,CDK1,and the overexpression of CDKN1A,the inhibition of the cancer cell cycle,and the P53 signaling pathway.CONCLUSION MAJ100 has great potential to decrease the activity and induce apoptosis in MDA-MB-231 cells via a variety of targets and pathways.