Icariin induces apoptosis in breast cancer MCF-7 cells by regulating the MELK mediated PI3K/AKT signaling pathway

Objective: To investigate the mechanism of icariin in promoting apoptosis of breast cancer cells by regulating the Phosphatidyli-nositol kinase (PI3K) PI3K/AKT signaling pathway mediated by Maternal embryonic leucine zipper kinase (MELK). Methods: Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting were used to detect the expression of MELK. small interfering RNA (siRNA)-MELK cell transfection technology was used to detect the correlation between MELK and PI3K/AKT. Different icariin concentrations on proliferation, migration and apoptosis of breast cancer cells were detected by flow cytometry, CCK-8, and Transwell. Western blot was used to detect the effects of icariin on MELK expression, AKT, cyclin, and apoptosis-related proteins. Results: Compared with normal mammary epithelial cells, the expression of MELK in breast cancer cells was significantly increased (p < 0.01). si-MELK decreased the expression of p-AKT, increased the expression of epithelial-mesenchymal transition (EMT)-related protein E-cadherin, and decreased the expression of N-cadherin and vi-mentin. Compared with the control group, icariin solution group showed a decrease in cell proliferation ability, a significant increase in cell apoptosis and a decrease in cell migration ability (p < 0.05). Icariin could induce G2/M arrest and inhibit the growth of breast cancer cells. Conclusion: Icariin can inhibit the expression of MELK, inhibit the PI3k/AKT signaling pathway to a certain extent, and further has a therapeutic effect on breast cancer.

Icariin; Breast cancer; MELK; PI3K/AKT signaling pathway

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