What does this research mean for the field?

Luteolin dose-dependently inhibits proliferation and promotes apoptosis in breast cancer cells by suppressing the phosphorylation of the EGFR/STAT3/Akt pathway and inducing reactive oxygen species accumulation. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This study investigates luteolin's effects on breast cancer cell proliferation and apoptosis via specific molecular pathways.

May 17, 2026Open Access

Effects of luteolin on proliferation and apoptosis of breast cancer cells by regulating EGFR/STAT3/AKt pathway

Puntos clave

This study investigates luteolin's effects on breast cancer cell proliferation and apoptosis via specific molecular pathways.
Using MCF-7 breast cancer cells as the model, various doses of luteolin (5-45 μmol/L) were administered to assess effects on cell behavior.
Proliferation activity, apoptosis rate, reactive oxygen species levels, and protein expression were measured after treatment with luteolin or DMSO control.
Significant statistical analysis was performed with p-values to validate findings.
Luteolin at concentrations of 25, 35, and 45 μmol/L significantly reduced MCF-7 cell proliferation (P < 0.05).
The apoptosis rate and ROS levels increased significantly (P < 0.05) with luteolin treatment.
Luteolin downregulated p-EGFR, p-STAT3, and p-Akt expression (P < 0.05), indicating a specific inhibition of the EGFR/STAT3/Akt pathway.

Resumen

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.

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