VI-14, a novel flavonoid derivative, inhibits migration and invasion of human breast cancer cells |
| |
Authors: | Li Fanni Li Chenglin Zhang Haiwei Lu Zhijian Li Zhiyu You Qidong Lu Na Guo Qinglong |
| |
Affiliation: | a State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing 210009, People's Republic of Chinab Department of Medicinal Chemistry, China Pharmaceutical University, Nanjing 210009, People's Republic of China |
| |
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. |
| |
Keywords: | MTT, 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-diphenytetrazoliumromide MMP, matrix metalloproteinase TIMP, tissue inhibitor of metalloproteinase ECM, extracellular matrix MAPK, mitogen-activated protein kinase ERK, extracellular signal-regulated kinase JNK, c-Jun N-terminal kinase AP-1, activator protein-1 NF-κB, nuclear factor-kappa B |
本文献已被 ScienceDirect PubMed 等数据库收录! |
|