Puerarin Inhibits Proliferation, Migration and Invasion of Colon Cancer Cells and Induces Apoptosis via Suppression of the PI3K/AKT Signaling Pathway

作者：Lin Chen, Xuhong Li, Shijie Zhao, Mengyu Hao, Heng Wang, Zhi Zhou, Xinyu Xiong, Die Yuan, Piao Luo, Luwen Wang, Di Pan, Xiangchun Shen, Yue Zhang, Yan Chen · 发表于：Pharmaceuticals · 年份：2025 · DOI：10.3390/ph18091378 · 被引用次数：4 · 研究领域：Phytoestrogen effects and research、Cancer, Lipids, and Metabolism、Cancer Research and Treatments

Background: Colon cancer is one of the most prevalent gastrointestinal malignancies worldwide, with high mortality and limited therapeutic options. Puerarin, a flavonoid compound derived from Pueraria lobata, has shown anticancer potential, but its molecular mechanisms against colon cancer remain unclear. Methods and Results: In this study, human colon cancer Caco-2 cells were treated with various concentrations of puerarin. Cell proliferation, migration, invasion, epithelial–mesenchymal transition (EMT), and apoptosis were evaluated using CCK-8, wound healing, Transwell, immunofluorescence, flow cytometry, and Western blot assays. Puerarin significantly inhibited Caco-2 cell proliferation in a dose- and time-dependent manner. It suppressed migration and invasion by increasing E-cadherin and reducing Vimentin expression. Apoptosis was induced via upregulation of BAX and downregulation of Bcl-2. Network pharmacology and KEGG analysis suggested PI3K/AKT signaling as a core regulatory pathway. Western blotting confirmed that puerarin reduced phosphorylation of PI3K and AKT. PI3K activator 740 Y-P promoted EMT and inhibited apoptosis, whereas puerarin and the PI3K inhibitor LY294002 reversed these effects. Conclusions: Puerarin exerts significant antitumor effects on Caco-2 colon cancer cells by inhibiting proliferation, migration, and EMT, while promoting apoptosis. These effects are mediated primarily through suppression of the PI3K/AKT signaling pathway. This study provides a ...