IMR Press / EJGO / Volume 42 / Issue 5 / DOI: 10.31083/j.ejgo4205144
Open Access Original Research
Icariin induces apoptosis in breast cancer MCF-7 cells by regulating the MELK mediated PI3K/AKT signaling pathway
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1 First Clinical Medical College, Nanjing University of Chinese Medicine, 210023 Nanjing, Jiangsu, China
2 Department of Oncology, Changzhou NO.2 People’s Hospital, 213000 Changzhou, Jiangsu, China
3 Department of Oncology, Jurong Hospital Affiliated to Jiangsu University, 212400 Jurong, Jiangsu, China
4 Department of Tumor Radiotherapy, The Affiliated Jiangning Hospital of Nanjing Medical University, 211100 Nanjing, Jiangsu, China
5 Department of Oncology, Rugao People’s Hospital, 210000 Rugao, Jiangsu, China
6 Department of Rheumatology and Immunology, Jinling Hospital, Medical school of Nanjing University, 210002 Nanjing, Jiangsu, China
Eur. J. Gynaecol. Oncol. 2021, 42(5), 957–965;
Submitted: 3 March 2021 | Revised: 31 March 2021 | Accepted: 26 April 2021 | Published: 15 October 2021

Objective: To investigate the mechanism of icariin in promoting apoptosis of breast cancer cells by regulating the Phosphatidylinositol 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 vimentin. 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.

Breast cancer
PI3K/AKT signaling pathway
Fig. 1.
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