Myricetin suppresses TGF-β-induced epithelial-to-mesenchymal transition in ovarian cancer

作者：Hui‐Wen Yang, Lan Yan, Li An, Han Wu, Ziwei Song, Ailing Wan, Yue Wang, Shibao Li, Shuai Ji, Zhongcheng Wang, Xinyu Wu, Ting Lan · 发表于：Frontiers in Pharmacology · 年份：2023 · DOI：10.3389/fphar.2023.1288883 · 被引用次数：15 · 研究领域：Kruppel-like factors research、Ovarian cancer diagnosis and treatment、FOXO transcription factor regulation

Background: Ovarian cancer (OC) is the second most common gynecological malignancy and has a high mortality rate. The current chemotherapeutic drugs have the disadvantages of drug resistance and side effects. Myricetin, a kind of natural compound, has the advantages of easy extraction, low price, and fewer side effects. Multiple studies have demonstrated the anti-cancer properties of myricetin. However, its impact on OC is still unknown and needs further investigation. Therefore, this study aimed to elucidate the mechanism by which myricetin suppresses transforming growth factor-β (TGF-β) -induced epithelial-to-mesenchymal transition (EMT) in OC through in vivo and in vitro experiments. Methods: In vitro experiments were conducted to evaluate the effects of myricetin on cell proliferation and apoptosis using CCK8 assay, plate clonal formation assay, and flow cytometry. Western blot was employed to evaluate the expression levels of caspase-3, PARP, and the MAPK/ERK and PI3K/AKT signaling pathways. Wound healing, transwell, western blot and immunofluorescence assay were used to detect TGF-β-induced cell migration, invasion, EMT and the levels of Smad3, MAPK/ERK, PI3K/AKT signaling pathways. Additionally, a mouse xenograft model was established to verify the effects of myricetin on OC in vivo . Results: Myricetin inhibited OC proliferation through MAPK/ERK and PI3K/AKT signaling pathways. Flow cytometry and western blot analyses demonstrated that myricetin promoted apoptosis by ...