Abstract
Metastasis is the major cause of death in breast cancer patients. In this study, we investigated the effects of baicalin, a natural compound, on cell migration, invasion and metastasis using human breast cancer MDA-MB-231 cell line as model system. Baicalin not only dose-dependently inhibited MDA-MB-231 cells migration and in vitro invasion, but also suppressed the tumor outgrowth and the pulmonary metastasis of MDA-MB-231 cells in xenograft model. Importantly, treatment of baicalin caused little change in body weight, liver and kidney function of recipient animals. Tumorigenesis-inhibitory effect is likely linked to the capability of baicalin to downregulate metalloproteinase (MMP)-2, MMP-9, urokinase-type plasminogen activator (uPA) and uPA receptor (uPAR) expression in MDA-MB-231 cells. As baicalin blocked p38 mitogen-activated protein kinase (MAPK) activity and treatment of p38MAPK inhibitor SB203580 led to the reduction of MMP-2, MMP-9, uPA and uPAR expressions, we concluded that baicalin suppresses the tumorigenecity of MDA-MB-231 cells by down-regulating MMP-2, MMP-9, uPA and uPAR expressions through the interruption of p38MAPK signaling pathway.
Keywords: Baicalin, breast cancer, MDA-MB-231 cell, metastasis, side effects.
Anti-Cancer Agents in Medicinal Chemistry
Title:Baicalin Suppresses Migration, Invasion and Metastasis of Breast Cancer via p38MAPK Signaling Pathway
Volume: 13 Issue: 6
Author(s): Xiu- Feng Wang, Qian- Mei Zhou, Jia Du, Hui Zhang, Yi- Yu Lu and Shi- Bing Su
Affiliation:
Keywords: Baicalin, breast cancer, MDA-MB-231 cell, metastasis, side effects.
Abstract: Metastasis is the major cause of death in breast cancer patients. In this study, we investigated the effects of baicalin, a natural compound, on cell migration, invasion and metastasis using human breast cancer MDA-MB-231 cell line as model system. Baicalin not only dose-dependently inhibited MDA-MB-231 cells migration and in vitro invasion, but also suppressed the tumor outgrowth and the pulmonary metastasis of MDA-MB-231 cells in xenograft model. Importantly, treatment of baicalin caused little change in body weight, liver and kidney function of recipient animals. Tumorigenesis-inhibitory effect is likely linked to the capability of baicalin to downregulate metalloproteinase (MMP)-2, MMP-9, urokinase-type plasminogen activator (uPA) and uPA receptor (uPAR) expression in MDA-MB-231 cells. As baicalin blocked p38 mitogen-activated protein kinase (MAPK) activity and treatment of p38MAPK inhibitor SB203580 led to the reduction of MMP-2, MMP-9, uPA and uPAR expressions, we concluded that baicalin suppresses the tumorigenecity of MDA-MB-231 cells by down-regulating MMP-2, MMP-9, uPA and uPAR expressions through the interruption of p38MAPK signaling pathway.
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Wang Feng Xiu-, Zhou Mei Qian-, Du Jia, Zhang Hui, Lu Yu Yi- and Su Bing Shi-, Baicalin Suppresses Migration, Invasion and Metastasis of Breast Cancer via p38MAPK Signaling Pathway, Anti-Cancer Agents in Medicinal Chemistry 2013; 13 (6) . https://dx.doi.org/10.2174/18715206113139990143
DOI https://dx.doi.org/10.2174/18715206113139990143 |
Print ISSN 1871-5206 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5992 |
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