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.
Export Options
About this article
Cite this article as:
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 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Oleuropein Mediated Targeting of Signaling Network in Cancer
Current Topics in Medicinal Chemistry Adopting Network Pharmacology for Cancer Drug Discovery
Current Drug Discovery Technologies Urate Transport: Regulators of Serum Urate Levels in Humans
Current Rheumatology Reviews Genetic and Epigenetic Regulation of Phosphoinositide 3-kinase Isoforms
Current Pharmaceutical Design Polypharmacological Properties and Therapeutic Potential of β-Caryophyllene: A Dietary Phytocannabinoid of Pharmaceutical Promise
Current Pharmaceutical Design Bisacylimidoselenocarbamates Cause G2/M Arrest Associated with the Modulation of CDK1 and Chk2 in Human Breast Cancer MCF-7 Cells
Current Medicinal Chemistry Neuro-endocrine Markers in Neoplasms. Diagnostic Interest and Future Prospects
Current Proteomics Integrins as Novel Drug Targets for Overcoming Innate Drug Resistance
Current Cancer Drug Targets All for Statins and Statins for All; An Update
Current Pharmaceutical Design Radiopharmaceutical: Revolutionary Agents for Diagnosis
Current Radiopharmaceuticals Advancing the Therapeutic Efficacy of Bioactive Molecules by Delivery Vehicle Platforms
Current Medicinal Chemistry Anti-Cancer
Current Bioactive Compounds Molecular Aspects of Intestinal Radiation-Induced Fibrosis
Current Molecular Medicine Vitamin D Analogs as Modulators of Vitamin D Receptor Action
Current Topics in Medicinal Chemistry Effective Treatment of Human Lung Cancer by Targeting Tissue Factor with a Factor VII-Targeted Photodynamic Therapy
Current Cancer Drug Targets Passive Targeting of Cyclophosphamide-Loaded Carbonate Apatite Nanoparticles to Liver Impedes Breast Tumor Growth in a Syngeneic Model
Current Pharmaceutical Design Recent Patents on MicroRNA-Induced Pluripotent Stem Cell Generation
Recent Patents on Regenerative Medicine IL-17 and its Receptor Complex as Therapeutic Targets in Arthritis
Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Discontinued) Cancer Genetics and Drug Discovery in Mice
Letters in Drug Design & Discovery Recent Advance in the Design of Small Molecular Modulators of Estrogen-Related Receptors
Current Pharmaceutical Design