Abstract

Breast cancer is one of the most frequently occurring malignant tumors affecting women's health. At least one million new cases are diagnosed each year. Therefore, research that aims to identify strategies that inhibit the growth of breast cancer cells has become a primary worldwide focus. Traditional Chinese medicine (TCM) is regarded as a valuable resource in China, and numerous monomer compositions extracted from TCMs have been demonstrated to exhibit antitumor effects. The present study aimed to determine the impact of paeoniflorin (PF) on breast cancer cell proliferation and invasion, and to explore the mechanisms underlying its effects. Different concentrations of PF were applied to MCF‑7 cells at various time points and the Cell Counting kit‑8 assay was used to determine cell proliferation, a transwell invasion assay was employed to determine cell invasion, reverse transcription‑polymerase chain reaction was used to determine notch homolog‑1 (NOTCH‑1) and Hes family basic helix‑loop helix transcription factor (HES)‑1 mRNA expression levels, and western blotting was used to determine NOTCH‑1 and HES‑1 protein expression levels. The results demonstrated that PF inhibited the proliferation of MCF‑7 cells in a dose‑ and time‑dependent manner. Following treatment with different concentrations of PF, the total number of cells present in the PF‑treated groups was significantly lower when compared with the untreated control group (P<0.05). With increasing doses of PF, the rate of cell invasion significantly decreased, indicating a dose‑dependent association. NOTCH‑1 and HES‑1 mRNA expression levels were reduced when compared with the untreated control group, which reached a statistical significance following treatment with 15 and 30µM PF (P<0.05). NOTCH‑1 and HES‑1 protein levels demonstrated a similar trend to the mRNA levels, whereby an increase in the concentration of PF was associated with a decrease in NOTCH‑1 and HES‑1 protein expression levels. The results of the present study therefore suggest that PF may inhibit the proliferation and invasiveness of breast cancer cells via inhibition of the NOTCH‑1 signaling pathway.

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