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Article Publish Status: FREE
Abstract Title:

A novel anticancer property ofpolysaccharide in triggering ferroptosis of breast cancer cells.

Abstract Source:

J Zhejiang Univ Sci B. 2022 Apr 15 ;23(4):286-299. PMID: 35403384

Abstract Author(s):

Xing DU, Jingjing Zhang, Ling Liu, Bo Xu, Hang Han, Wenjie Dai, Xiuying Pei, Xufeng Fu, Shaozhang Hou

Article Affiliation:

Xing DU

Abstract:

Breast cancer is one of the most malignant tumors and is associated with high mortality rates among women.polysaccharide (LBP) is an extract from the fruits of the traditional Chinese herb,. LBP is a promising anticancer drug, due to its high activity and low toxicity. Although it has anticancer properties, its mechanisms of action have not been fully established. Ferroptosis, which is a novel anticancer strategy, is a cell death mechanism that relies on iron-dependent lipid reactive oxygen species (ROS) accumulation. In this study, human breast cancer cells (Michigan Cancer Foundation-7 (MCF-7) and MD Anderson-Metastatic Breast-231 (MDA-MB-231)) were treated with LBP. LBP inhibited their viability and proliferation in association with high levels of ferroptosis. Therefore, we aimed to ascertain whether LBP reduced cell viability through ferroptosis. We found that the structure and function of mitochondria, lipid peroxidation, and expression of solute carrier family 7 member 11 (SLC7A11, also known as xCT, the light-chain subunit of cystine/glutamate antiporter system X) and glutathione peroxidase 4 (GPX4) were altered by LBP. Moreover, the ferroptosis inhibitor, Ferrostatin-1 (Fer-1), rescued LBP-induced ferroptosis-associated events including reduced cell viability and glutathione (GSH) production, accumulation of intracellular free divalent iron ions and malondialdehyde (MDA), and down-regulation of the expression of xCT and GPX4. Erastin (xCT inhibitor) and RSL3 (GPX4 inhibitor) inhibited the expression of xCT and GPX4, respectively, which was lower after the co-treatment of LBP with Erastin and RSL3. These results suggest that LBP effectively prevents breast cancer cell proliferation and promotes ferroptosis via the xCT/GPX4 pathway. Therefore, LBP exhibits novel anticancer properties by triggering ferroptosis, and may be a potential therapeutic option for breast cancer.

Study Type : In Vitro Study

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