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Fusaric acid inhibits proliferation and induces apoptosis through triggering endoplasmic reticulum stress in MCF-7 human breast cancer cells

文献类型: 外文期刊

作者: Zhang, Jun 1 ; Yuan, Huikai 2 ; Li, Wei 2 ; Chen, Shuo 3 ; Liu, Siwen 4 ; Li, Chunyu 4 ; Yao, Xiaoqiang 1 ;

作者机构: 1.Chinese Univ Hong Kong, Li Ka Shing Inst Hlth Sci, Sch Biomed Sci, Hong Kong, Peoples R China

2.Harbin Med Univ, Affiliated Hosp 1, Dept Gen Surg, Harbin, Peoples R China

3.Harbin Med Univ Daqing, Sch Pharm, Dept Biopharmaceut Sci, Daqing, Peoples R China

4.Guangdong Acad Agr Sci, Guangdong Prov Key Lab Trop & Subtrop Fruit Tree R, Key Lab South Subtrop Fruit Biol & Genet Res Utili, Minist Agr & Rural Affairs,Inst Fruit Tree Res, Guangzhou, Peoples R China

5.Chinese Univ Hong, Lo Kwee-Seong Integrated Biomed Sci Bldg, Rm 224A, Area 39, Hong Kong, Peoples R China

关键词: Fusaric acid; Breast cancer; MCF-7 cells; Cell cycle arrest; Apoptosis; ER stress

期刊名称:MYCOTOXIN RESEARCH ( 影响因子:3.0; 五年影响因子:3.9 )

ISSN: 0178-7888

年卷期: 2023 年

页码:

收录情况: SCI

摘要: Breast cancer has replaced lung cancer to be the leading cancer in the world. Currently, chemotherapy is still the major method for breast cancer therapy, but its overall effect remains unsatisfactory. Fusaric acid (FSA), a mycotoxin derived from fusarium species, has shown potency against the proliferation of several types of cancer cells, but its effect on breast cancer cells has not been examined. Therefore, we explored the possible effect of FSA on the proliferation of MCF-7 human breast cancer cells and uncovered the underlying mechanism in the present study. Our results showed that FSA has a strong anti-proliferative effect on MCF-7 cells through inducing ROS production, apoptosis and arresting cell cycle at G2/M transition phase. Additionally, FSA triggers endoplasmic reticulum (ER) stress in the cells. Notably, the cell cycle arrest and apoptosis inducing effect of FSA can be attenuated by ER stress inhibitor, tauroursodeoxycholic acid. Our study provide evidence that FSA is a potent proliferation inhibition and apoptosis inducing agent against human breast cancer cells, and the possible mechanism involves the activation of ER stress signaling pathways. Our study may highlight that FSA is promising for the future in vivo study and development of potential agent for breast cancer therapy.

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