Abstract Breast cancer (BC) is a common malignant tumor in women, characterized by high recurrence rates, a significant risk of metastasis, and limitations of existing treatments. The anticancer activity of the natural compound luteolin (LU) has been confirmed, but its specific mechanism of action in breast cancer cells (BCCs) has not been fully elucidated. This study aimed to investigate the effects of LU on the proliferation and apoptosis of BCCs and to clarify its association with the epidermal growth factor receptor (EGFR)/signal transducer and activator of transcription 3 (STAT3)/protein kinase B (Akt) pathway. Using MCF-7 breast cancer cells as the research subject, experimental groups were set up with 5, 15, 25, 35, and 45 μmol/L LU treatment and a dimethyl sulfoxide (DMSO) solvent control group. Cell proliferation activity, reactive oxygen species (ROS) levels, apoptosis rate (AR), and the expression of phosphorylated Akt (p-Akt), phosphorylated EGFR (p-EGFR), and phosphorylated STAT3 (p-STAT3) were detected. LU at concentrations of 25, 35, and 45 μmol/L significantly inhibited the proliferation of MCF-7 cells ( P 0.05). The inhibitory effect of LU on MCF-7 cell proliferation and its pro-apoptotic effect were dose-dependent, with half-maximal inhibitory concentrations (IC 50 ) of 28.7 ± 1.5 μmol/L and 29.4 ± 1.8 μmol/L, respectively. LU dose-dependently inhibits the proliferation and promotes the apoptosis of MCF-7 cells by specifically inhibiting the phosphorylation activation of the EGFR/STAT3/Akt pathway and inducing ROS accumulation. This provides experimental evidence for LU as a potential therapeutic agent for breast cancer.
Zheng et al. (Thu,) studied this question.