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Keywords:icariin; triple-negative breast cancer; TGF-β/Smad; invasion and metastasis; epithelial-mesenchymal transition; molecular mechanisms;
DOI:10.19405/j.cnki.issn1000-1492.2025.09.002
〔Abstract〕 Objective To investigate the mechanism by which icariin(ICA) inhibits the invasion and metastasis of human triple-negative breast cancer(TNBC) cells via downregulation of the transforming growth factor-β/Smad(TGF-β/Smad) signaling pathway. Methods TNBC cells(MDA-MB-231 and MDA-MB-468) were cultured in vitro and divided into four groups: an experimental group treated with 15 μmol/L ICA; a model group treated with10 μmol/L TGF-β receptor inhibitor LY2109761; a combination group(LY2109761 + ICA) treated with both 15μmol/L ICA and 10 μmol/L LY2109761; and a control group. Cell proliferation,migration,and invasion were assessed using CCK-8,colony formation,5-ethynyl-2'-deoxyuridine(EdU),wound healing,and Transwell assays.The expression levels of epithelial-mesenchymal transition(EMT)-related proteins,as well as TGF-β1,Smad2,and phosphorylated Smad2(P-Smad2) were detected by immunofluorescence and Western blot. Results CCK-8 results showed that cell proliferation decreased gradually with increasing concentrations of ICA(P