Effects of phloretin on the proliferation,apoptosis,and tumorigenicity of ovarian cancer cells by regulating Rac1/Akt/NF-κB signaling pathway
10.12007/j.issn.0258-4646.2025.09.010
- VernacularTitle:根皮素通过调节Rac1/Akt/NF-κB信号通路对卵巢癌细胞增殖、凋亡和致瘤性的影响
- Author:
Yuehong TANG
1
;
Yuning LUO
1
;
Libin XU
1
;
Xiaoying HU
1
;
Chunping QIU
1
Author Information
1. 海南省妇产科医院妇产科,海口 570100
- Publication Type:Journal Article
- Keywords:
phloretin;
Rac1/Akt/NF-κB signaling pathway;
proliferation;
tumorigenicity;
apoptosis
- From:
Journal of China Medical University
2025;54(9):821-825,831
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of phloretin on the proliferation,apoptosis,and tumorigenicity of ovarian cancer cells by regu-lating the Rac1/Akt/NF-κB signaling pathway.Methods The ovarian cancer cell line SKOV3 and the human normal ovarian epithelial cell line IOSE-80 were divided into the following groups:control,low-dose phloretin,medium-dose phloretin,high-dose phloretin,PM A,and high-dose phloretin+PMA.Morphological changes were observed under a microscope.Cell viability and apoptosis were assessed using the CCK-8 assay,colony formation assay,and flow cytometry.Western blotting was performed to detect the expression of proteins related to the Rac1/Akt/NF-κB signaling pathway.Tumor-bearing nude mice were established,tumor weights were measured,and the expres-sion levels of Rae1 and Akt in tumor tissues were analyzed.Results Compared with the control group,SKOV3 cells treated with low-,medium-,and high-dose phloretin showed reduced survival rate,colony formation,and expression of p-NF-κB p65/NF-κB p65,p-Akt/Akt,and Rac 1 in a dose-dependent manner.However,PM A reversed the inhibitory effects of high-dose phloretin on the malignant progression of ovarian cancer.In vivo experiments demonstrated that phloretin significantly inhibited tumor growth and reduced Akt and Rae1 expres-sion in tumor tissues(P<0.05).Conclusion Phloretin suppresses the malignant progression of ovarian cancer by inhibiting the Rae1/Akt/NF-κB signaling pathway.