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Journal of Cancer Prevention

Original Article

J Cancer Prev 2021; 26(3): 183-194

Published online September 30, 2021

https://doi.org/10.15430/JCP.2021.26.3.183

© Korean Society of Cancer Prevention

Dioscin Decreases Breast Cancer Stem-like Cell Proliferation via Cell Cycle Arrest by Modulating p38 Mitogen-activated Protein Kinase and AKT/mTOR Signaling Pathways

Chae Won Ock1,2 , Gi Dae Kim2

1College of Pharmacy, Natural Products Research Institute, Seoul National University, Seoul, 2Department of Food and Nutrition, Kyungnam University, Changwon, Korea

Correspondence to :
Gi Dae Kim, E-mail: gidaekim@kyungnam.ac.kr, https://orcid.org/0000-0002-8149-5361

Received: August 30, 2021; Revised: September 14, 2021; Accepted: September 15, 2021

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Dioscin (DS), a steroidal saponin, has been shown to have anti-cancer activity by exerting antioxidant effects and inducing apoptosis. However, the anti-cancer activity of DS in breast cancer-derived stem cells is still controversial. The purpose of this study was to evaluate the effects of DS on migration, invasion, and colony formation in MDA-MB-231 and MCF-7 cell lines and the mechanism by which it inhibits proliferation of breast cancer stem-like cells after inducing differentiation into breast cancer stem cells. DS treatment significantly reduced cellular migration, invasion, and colony formation in MDA-MB-231 and MCF-7 cells. During the differentiation process that induced manifestation of breast cancer stem-like cells, DS significantly inhibited mammosphere formation in a dose-dependent manner and increased the expression of p53 and p21 in breast cancer stem-like cells, reducing the expression of cdc2 and cyclin B1 in MDA-MB-231 cells and cyclin D, cyclin E, CDK4, and CDK2 in MCF-7 cells. Interestingly, DS treatment induced G2/M and G0/G1 cell cycle arrest in the MDA-MB-231 and MCF-7 cells, respectively. DS also increased the phosphorylation of p38 and decreased the expression levels of p-AKT and p-mTOR. These results suggest that DS regulates the p38 mitogen-activated protein kinase and AKT/mTOR signaling pathways to reduce the proliferation of breast cancer stem-like cells through cell cycle arrest. Therefore, these findings suggest that DS may serve as a potential treatment candidate targeting breast cancer stem cells.

Keywords: Dioscin, Breast cancer, AKT/mTOR

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