磷脂酰肌醇3-激酶/AKT/哺乳动物雷帕霉素靶向(mTOR)信号通路是一条复杂的细胞内代谢通路，导致细胞增殖和肿瘤增殖，并在乳腺癌的药物耐药性中发挥关键作用。因此，研究雄烯酸(OA)、橄榄酸(MA)及其组合的抗癌效应，以提高治疗策略的性能。我们使用WST-1方法研究了OA和MA对细胞存活力的影响。采用等剂量图分析方法分析了组合的协同效应。此外，还通过定量RT-PCR分析了两种化合物在MCF7细胞中对凋亡、自噬和细胞周期的影响。此外，还通过定量RT-PCR确定了参与细胞凋亡、细胞周期和代谢的PI3K/AKT/mTOR基因表达的变化。 MA、OA和两者的组合均导致G0/G1阻滞。所有治疗组的细胞凋亡也增加。MA处理组的自噬小体LC3-II形成增加了1.74倍，而MA-OA处理组增加了3.25倍。组合治疗导致GSK3B、PTEN、CDKN1B和FOXO3等基因的表达增加，并导致IGF1、PRKCB和AKT3等基因的表达减少。 结果显示，这两种物质的组合在最低剂量下表现出最高的协同效应，并且使用MA-OA导致癌细胞发生凋亡。使用组合药物可能降低癌细胞对治疗的耐药性。©2023 作者。

The phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin (PI3K/AKT/ mTOR) pathway is a complex intracellular metabolic pathway that leads to cell growth and tumor proliferation and plays a key role in drug resistance in breast cancer. Therefore, the anti-cancer effects of oleanolic acid (OA), maslinic acid (MA), and their combination were investigated to improve the performance of the treatment strategy.We investigated the effect of OA and MA on cell viability using the WST-1 method. The synergistic effect of the combination was analyzed by isobologram analysis. In addition, the effects of the two compounds, individually and in combination, on apoptosis, autophagy, and the cell cycle were investigated in MCF7 cells. In addition, changes in the expression of PI3K/AKT/mTOR genes involved in apoptosis, cell cycle and metabolism were determined by quantitative RT-PCR.MA, OA, and a combination of both caused G0/G1 arrest. Apoptosis also increased in all treated groups. The autophagosomal LC3-II formation was induced 1.74-fold in the MA-treated group and 3.25-fold in the MA-OA-treated group. The combination treatment resulted in increased expression of genes such as GSK3B, PTEN, CDKN1B and FOXO3 and decreased expression of IGF1, PRKCB and AKT3 genes.The results showed that the combination of these two substances showed the highest synergistic effect at the lowest dose and using MA-OA caused cancer cells to undergo apoptosis. The use of combination drugs may reduce the resistance of cancer cells to treatment.©2023 The Authors.