Open Access


Read more
image01

Online Manuscript Submission


Read more
image01

Submitted Manuscript Trail


Read more
image01

Online Payment


Read more
image01

Online Subscription


Read more
image01

Email Alert



Read more
image01

Original Research Article | OPEN ACCESS

Ginsenoside induces cell death in breast cancer cells via ROS/PI3K/Akt signaling pathway

Lihong He1, Xiaorui Wang1, Qing Ma2, Weipeng Zhao1, Yongsheng Jia1, Guolei Dong1, Yuehong Zhu1, Xiaochen Jia1, Zhongsheng Tong1

1Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital; 2Department of Oncology, General Hospital of Tianjin Medical University, Tianjin, PR China.

For correspondence:-  Zhongsheng Tong   Email: msst19@163.com

Accepted: 2 August 2020        Published: 31 August 2020

Citation: He L, Wang X, Ma Q, Zhao W, Jia Y, Dong G, et al. Ginsenoside induces cell death in breast cancer cells via ROS/PI3K/Akt signaling pathway. Trop J Pharm Res 2020; 19(8):1631-1636 doi: 10.4314/tjpr.v19i8.10

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To study the influence of ginsenoside on breast carcinoma, and the mechanism of action involved.
Methods: Different concentrations of ginsenoside were used to treat MCF-7 breast cancer cell line. Cell viability was measured by MTT assay, while protein expressions of p-Akt and p-PI3K were determined using Western blotting. The concentrations of reactive oxidative reactants and reactive oxygen species (ROS) were assessed using fluorescence immunoassay and immunofluorescence assay. The mechanism of action involved in ginsenoside-mediated apoptosis was determined based on ROS/PI3K/Akt signaling pathway.
Results: There was no change in the inhibition of MCF-7 cell proliferation in control cells with time (p > 0.05). However, inhibition of MCF-7 cell proliferation in ginsenoside group was significantly higher than that in the control group (p < 0.05); furthermore, it increased with time and ginsenoside concentration. Apoptosis was markedly and concentration-dependently higher in ginsenoside-treated MCF-7 cells than in controls (p > 0.05). There were lower protein levels of p-PI3K and p-Akt in ginsenoside-exposed MCF-7 cells than in control group; the protein expressions decreased with increase in ginsenoside concentration (p < 0.05). The expressions of ROS in ginsenoside-treated MCF-7 cells declined, relative to the untreated group; in addition, the expressions decreased with increase in ginsenoside concentration (p < 0.05).
Conclusion: Ginsenoside suppresses proliferation of MCF-7 cell line, and exerts apoptotic effect on the cells via inhibition of the ROS/PI3K/Akt signal pathway. This provides a new approach to treat breast cancer.

Keywords: Breast cancer cells, Ginsenoside, Apoptosis, ROS/PI3K/Akt signaling pathway

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

Article Tools

Share this article with



Article status: Free
Fulltext in PDF
Similar articles in Google
Similar article in this Journal:

Archives

2024; 23: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10
2023; 22: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2022; 21: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2021; 20: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2020; 19: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2019; 18: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2018; 17: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2017; 16: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2016; 15: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2015; 14: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2014; 13: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2013; 12: 
1,   2,   3,   4,   5,   6
2012; 11: 
1,   2,   3,   4,   5,   6
2011; 10: 
1,   2,   3,   4,   5,   6
2010; 9: 
1,   2,   3,   4,   5,   6
2009; 8: 
1,   2,   3,   4,   5,   6
2008; 7: 
1,   2,   3,   4
2007; 6: 
1,   2,   3,   4
2006; 5: 
1,   2
2005; 4: 
1,   2
2004; 3: 
1
2003; 2: 
1,   2
2002; 1: 
1,   2

News Updates