Open AccessEpigallocatechin-3-gallate inhibits the proliferation and migration of human ovarian carcinoma cells by modulating p38 kinase and matrix metalloproteinase-2
Author(s) -
Feng Wang,
Zhiwei Chang,
Qingxia Fan,
Liuxing Wang
Publication year - 2014
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2014.1909
Subject(s) - p38 mitogen activated protein kinases , cell growth , mapk/erk pathway , kinase , mtt assay , protein kinase a , cell cycle , biology , microbiology and biotechnology , cancer research , gentamicin protection assay , chemistry , cell , western blot , biochemistry , gene
Epigallocatechin‑3‑gallate (EGCG), a major catechin in green tea, has recently been reported to exhibit anticancer effects on a number of types of cancer cells in vitro; however, the molecular mechanisms of this anticancer effect remain poorly understood. In the current study, the effects of EGCG on the proliferation and migration of the OVCAR‑3 human ovarian carcinoma cell line were investigated. Cells were treated with EGCG and their proliferation rates were determined by an MTT assay. In addition, cell migration was detected by transwell assay. The activity of mitogen‑activated protein kinases (MAPKs) and the expression of matrix metalloproteinase‑2/9 (MMP‑2/9) were examined by western blotting. The results showed that EGCG significantly inhibited (P<0.05) the proliferation of OVCAR‑3 cells in a time‑ and concentration‑dependent manner. EGCG (100 µM) time‑dependently increased (P<0.05) the activity of p38, but not extracellular signal‑regulated kinases 1/2. SB203580, a specific p38 MAPK inhibitor, completely diminished EGCG‑induced phosphorylation of p38 and partially blocked EGCG‑inhibited OVCAR‑3 cell proliferation. Furthermore, EGCG (0‑100 µM) dose‑dependently inhibited (P<0.05) OVCAR‑3 cell migration. The protein expression levels of MPP‑2, but not MMP‑9, were dose‑dependently decreased following treatment with EGCG (0‑100 µM) for 48 h. These data indicated that EGCG inhibited OVCAR‑3 cell proliferation and migration, potentially mediated via the activation of p38 MAPK and downregulation of the protein expression of MMP2. Thus, the therapeutic potential of EGCG for ovarian cancer requires further investigation.