The Analysis of the Anti-Tumor Mechanism of Ursolic Acid Using Connectively Map Approach in Breast Cancer Cells Line MCF-7
Authors Guo W, Xu B, Wang X, Zheng B, Du J, Liu S
Received 11 December 2019
Accepted for publication 23 April 2020
Published 15 May 2020 Volume 2020:12 Pages 3469—3476
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Yong Teng
Weiqiang Guo,1 Bin Xu,1 Xiaoxiao Wang,2 Bo Zheng,1 Jiahui Du,2 Songbai Liu2
1School of Chemistry, Biology and Material Engineering, Suzhou University of Science and Technology, Suzhou 215009, People’s Republic of China; 2Suzhou Key Laboratory for Medical Biotechnology, Suzhou Vocational Health College, Suzhou 215009, People’s Republic of China
Correspondence: Weiqiang Guo
School of Chemistry, Biology and Material Engineering, Suzhou University of Science and Technology, Suzhou 215009, People’s Republic of China
Suzhou Key Laboratory for Medical Biotechnology, Suzhou Vocational Health College, Suzhou 215009, People’s Republic of China
Background: Ursolic acid (UA), a primary bioactive triterpenoid, was reported as an anti-cancer agent. However, the current knowledge of UA and its potential anti-cancer mechanisms and targets in breast cancer cells are limited. In this study, we aimed to illustrate the potential mechanisms and targets of UA in breast cancer cells MCF-7.
Methods: The effect of UA on cell growth was determined in MCF-7 cells by MTT assay. The anti-tumor mechanism of UA was evaluated by microarray, CAMP, and Western blot. Moreover, the molecular docking between UA and potential receptors were predicted by iGEMDOCK software.
Results: The result of MTT assay demonstrated that UA could inhibit MCF-7 cell growth with IC50 values of 20 μM. Microarray and CMAP analysis, validated by Western blot, indicated that UA significantly modulated IKK/NF-κB, RAF/ERK pathways, and down-regulated the phosphorylation level of PLK1 in MCF-7 cells.
Conclusion: Our data indicated that the anti-tumor effects of UA are due to the inhibited RAF/ERK pathway and IKK/NF-κB pathway. It could also be explained by the reduced phosphorylation of PLK1 in MCF-7 cells. This study provides a new insight for deep understanding of the new anti-cancer mechanisms of UA in MCF-7 breast cancer cells.
Keywords: ursolic acid, connectivity map, RAF/ERK, IKK/NF-κB, PLK1
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