Found programs:
Authors:Liu Hancheng; Li Huiming; Zhang Jie; Meng Qinglai; Ding Shi; Ma Lihui
Keywords:eriodictyol;triple-negative breast cancer;proliferation;apoptosis;c-Myc;androgen recepter
DOI:10.19405/j.cnki.issn1000-1492.2022.06.009
〔Abstract〕 Objective To explore the effect of eriodictyol(Eri) on the proliferation and apoptosis of triple-negative breast cancer MDA-MB-231 cells and its possible mechanism. Methods MDA-MB-231 cells were treated with different concentrations of Eri. MTT method was used to detect the level of cell proliferation. Plate clone method was used to detect the the level of cell clonality. The apoptosis level was detected by flow cytometry. Western blot was used to detect protein expression levels of Cleaved-caspase-3, Bax, Bcl-2, c-Myc and AR. MDA-MB-231 cells were transfected with si-c-Myc and then combined treatment with 50 μmol/L Eri. MTT method was used to detect the level of cell proliferation. The apoptosis level was detected by flow cytometry. Western blot was used to detect protein expression levels of c-Myc and AR. Results Eri inhibited the proliferation activity of MDA-MB-231 cells in a dose and time-dependent manner. Treatment with different concentrations of Eri reduced cloning ability of MDA-MB-231 cells, promoted cell apoptosis, up-regulated the protein expression levels of Cleaved-caspase-3 and Bax, and down-regulated the protein expression level of Bcl-2, c-Myc and AR. Knockdown of c-Myc expression inhibited MDA-MB-231 cells growth, promoted cell apoptosis, and down-regulated the protein expression level of c-Myc and AR, while combined treatment with 50 μmol/L Eri could not enhance the situation. Conclusion Er inhibits proliferation and induces apoptosis in triple-negative breast cancer MDA-MB-231 cells, which may be achieved by inhibiting c-Myc/AR axis.