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Original Research

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

  • Danping Qian1,2
  • Yin Zhu3
  • Le Xu4
  • Tingting Dong1
  • Ting Chen5
  • Zhenghong Yu1,6,*,

1First Clinical Medical College, Nanjing University of Chinese Medicine, 210023 Nanjing, Jiangsu, China

2Department of Oncology, Changzhou NO.2 People's Hospital, 213000 Changzhou, Jiangsu, China

3Department of Oncology, Jurong Hospital Affiliated to Jiangsu University, 212400 Jurong, Jiangsu, China

4Department of Tumor Radiotherapy, The Affiliated Jiangning Hospital of Nanjing Medical University, 211100 Nanjing, Jiangsu, China

5Department of Oncology, Rugao People's Hospital, 210000 Rugao, Jiangsu, China

6Department of Rheumatology and Immunology, Jinling Hospital, Medical school of Nanjing University, 210002 Nanjing, Jiangsu, China

DOI: 10.31083/j.ejgo4205144 Vol.42,Issue 5,October 2021 pp.957-965

Submitted: 03 March 2021 Accepted: 26 April 2021

Published: 15 October 2021

*Corresponding Author(s): Zhenghong Yu E-mail: 13327800182@189.cn

Abstract

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.


Keywords

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


Cite and Share

Danping Qian,Yin Zhu,Le Xu,Tingting Dong,Ting Chen,Zhenghong Yu. Icariin induces apoptosis in breast cancer MCF-7 cells by regulating the MELK mediated PI3K/AKT signaling pathway. European Journal of Gynaecological Oncology. 2021. 42(5);957-965.

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