1. VI-14, a novel flavonoid derivative, inhibits migration and invasion of human breast cancer cells.
- Author
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Li F, Li C, Zhang H, Lu Z, Li Z, You Q, Lu N, and Guo Q
- Subjects
- Antineoplastic Agents chemistry, Breast Neoplasms pathology, Cell Line, Tumor, Cell Survival drug effects, Female, Flavonoids chemistry, Humans, MAP Kinase Signaling System drug effects, Matrix Metalloproteinase 2 genetics, Matrix Metalloproteinase 9 genetics, Neoplasm Invasiveness, Tissue Inhibitor of Metalloproteinase-1 analysis, Antineoplastic Agents pharmacology, Breast Neoplasms drug therapy, Cell Movement drug effects, Flavonoids pharmacology
- Abstract
It has been well characterized that flavonoids possess pronounced anticancer potentials including anti-angiogenesis, anti-metastasis, and pro-apoptosis. Herein, we report, for the first time, that VI-14, a novel flavonoid derivative, possesses anti-cancer properties. The purpose of this study is to investigate the anti-migration and anti-invasion activities of VI-14 in breast cancer cells. Our data indicate that VI-14 inhibits adhesion, migration and invasion of MDA-MB-231 and MDA-MB-435 human breast cancer cells. MDA-MB-231 cells treated with VI-14 display reduced activities and expressions of ECM degradation-associated proteins including matrix metalloproteinase 2 (MMP-2) and 9 (MMP-9) at both the protein and mRNA levels. Meanwhile, VI-14 treatment induces an up-regulated expression of tissue inhibitor of metalloproteinase 1 (TIMP-1) and 2 (TIMP-2) in MDA-MB-231 cells. Western blotting results show that phosphorylation levels of critical components of the MAPK signaling pathway, including ERK, JNK and P38, are dramatically decreased in VI-14-treated MDA-MB-231 cells. Furthermore, treatment of VI-14 significantly decreases the nuclear levels and the binding ability of nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1). Taken together, our data suggest that VI-14 treatment suppresses migration and motility of breast cancer cells, and VI-14 may be a potential compound for cancer therapy., (Copyright © 2012 Elsevier Inc. All rights reserved.)
- Published
- 2012
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