Emodin Inhibits the Proliferation of MCF-7 Human Breast Cancer Cells Through Activation of Aryl Hydrocarbon Receptor (AhR)

Frontiers in Pharmacology

Shuo Huang¹  Yanyan Tang¹  Shitang Ma²  Aimin Sheng³  Jiawen Wang⁴  Ge Hong⁵  Ning Zhang⁵ 

[1] Clinical College of Orthopedics, Tianjin Medical University, Tianjin Hospital, Tianjin, China;Life and Health College, Anhui Science and Technology University, Fengyang, China;School of Chemical Engineering, Anhui University of Science and Technology, Huainan, China;School of Pharmacy, East China University of Science and Technology, Shanghai, China;Tianjin Key Laboratory of Biomedical Materials, Institute of Biomedical Engineering, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China;

关键词: emodin;    AhR;    CYP1A1;    breast cancer;    MCF-7;    network pharmacology;   

DOI  :  10.3389/fphar.2020.622046

来源: DOAJ

【 摘 要 】

Natural products have proved to be a promising source for the development of potential anticancer drugs. Emodin, a natural compound from Rheum palmatum, is used to treat several types of cancers, including lung, liver, and pancreatic. However, there are few reports regarding its use in the treatment of breast cancer. Thus, the therapeutic effect and mechanism of emodin on MCF-7 human breast cancer cells were investigated in this study. Morphological observations and cell viability were evaluated to determine the anti-proliferation activity of emodin. Network pharmacology and molecular docking were performed to screen the potential targets. Western blot analysis was used to explore a potential antitumor mechanism. The results showed that emodin (50–100 μmol/L) could significantly inhibit the proliferation of MCF-7 cells in a time and dose-dependent manner. Furthermore, virtual screening studies indicated that emodin was a potent aryl hydrocarbon receptor (AhR) agonist in chemotherapy for breast cancer. Finally, when MCF-7 cells were treated with emodin (100 μmol/L) for 24 h, the AhR and cytochrome P450 1A1 (CYP1A1) protein expression levels were significantly upregulated compared with the control group. Our study indicated that emodin exhibited promising antitumor activity in MCF-7 cells, likely through activation of the AhR-CYP1A1 signaling pathway. These findings lay a foundation for the application of emodin in breast cancer treatment.

【 授权许可】

Unknown