Icariin inhibits the migration and invasion of triple negative breast cancer by down-regulating the TFG-β/ Smad signalling pathway
10.19405/j.cnki.issn1000-1492.2025.09.002
- VernacularTitle:淫羊藿苷下调 TGF-β/ Smad 信号通路 抑制三阴性乳腺癌侵袭转移
- Author:
Zengyou Xiao
1
;
Zean Yang
1
;
Caihong Chen
2
;
Jiaxian Li
3
;
Yujie He
3
;
Pinting Fu
3
;
Jie Wang
1
Author Information
1. Shanghai Putuo Central School of Clinical Medicine，Anhui Medical University，Shanghai 200062; Dept of Thyroid and Breast Surgery，Putuo Hospital，Shanghai University of Traditional Chinese Medicine，Shanghai 200062
2. Juquan New Town Community Health Service Center，Gucun Town，Baoshan District，Shanghai 200436
3. Dept of Thyroid and Breast Surgery，Putuo Hospital，Shanghai University of Traditional Chinese Medicine，Shanghai 200062
- Publication Type:Journal Article
- Keywords:
icariin;
triple-negative breast cancer;
TGF-β/Smad;
invasion and metastasis;
epithelial-mesenchymal transition;
molecular mechanisms
- From:
Acta Universitatis Medicinalis Anhui
2025;60(9):1574-1582
- CountryChina
- Language:Chinese
-
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 with 10 μmol / L TGF-β receptor inhibitor LY2109761; a combination group ( LY2109761 + ICA) treated with both 15 μmol / L ICA and 10 μmol / L LY2109761; and a control group．Cell proliferation，migration，and invasion were as- sessed 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＜0. 05) ．Colony formation and EdU assays indicated significantly inhibited proliferation in the ICA-treated group compared to the control ( P＜0. 05) ．Wound healing and Transwell assays demonstrated reduced migration and invasion capabilities in the experimental group relative to the control ( P＜0. 05) ．Compared to the model group，the LY2109761 + ICA group exhibited further suppression of invasion ( P＜0. 05) ．Immunofluorescence revealed decreased Vimentin ex- pression in the experimental group ( P＜0. 05) ，with an even more pronounced reduction in the LY2109761 + ICA group ( P＜0. 01) ．Western blot analysis showed that the protein levels of N-cadherin，matrix metalloproteinase-9( MMP9) ，Vimentin，TGF-β1，Smad2，and P-Smad2 were downregulated in the experimental group compared to the control ( P＜0. 05) ．These proteins were further suppressed in the LY2109761 + ICA group compared to the model group ( P＜0. 05) ．
Conclusion:ICA inhibits TNBC cells proliferation，invasion，metastasis，and EMT by downregulating the TGF-β/ Smad signaling pathway．
- Full text:2026031100124970331淫羊藿苷下调TGF-β_Smad信号通路抑制三阴性乳腺癌侵袭转移_肖增友.pdf
