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Updated: Oct 20, 2025

Indirect Immunofluorescence on Frozen Sections of Mouse Mammary Gland
Published on: December 1, 2015
Genistein Directly Represses the Phosphorylation of STAT5 in Lactating Mammary Epithelial Cells
Yusaku Tsugami1, Haruka Wakasa2, Takanori Nishimura2
1Laboratory of Animal Histophysiology, Graduate School of Integrated Sciences for Life, Hiroshima University, 1-4-4 Kagamiyama Higashi-Hiroshima 739-8528 Hiroshima, Japan.
Abstract:
Genistein is a soy isoflavone and shows various physiological activities, such as affinities for estrogen receptors (ERs) and inhibitory effects on the epidermal growth factor receptor (EGFR) pathway. A previous study reported that genistein downregulates milk production ability in mammary epithelial cells (MECs) while decreasing the phosphorylation of STAT5. The ER and EGFR pathways indirectly regulate STAT5. In this study, the repressing mechanism of genistein against the phosphorylation of STAT5 was investigated using a culture model of mouse MECs with milk production ability. The results revealed that genistein did not influence the behavior of ERα and ERβ, whereas genistein immediately repressed the phosphorylation of ERK1/2. However, the decrease in phosphorylated STAT5 occurred independent of the phosphorylation of EGFR. Genistein repressed new phosphorylation of STAT5 by prolactin without influencing the phosphorylation of JAK2. In conclusion, this study indicates that genistein directly inhibits the phosphorylation of STAT5 in lactating MECs.
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