posted on 2016-05-10, 00:00authored byT. Liu, P. Liu, F. Ding, N. Yu, S. Li, S. Wang, X. Zhang, X. Sun, Y. Chen, F. Wang, Y. Zhao, B. Li
Ampelopsin has displayed anticancer activity
in several types of cancers. However, no evidence has been
reported for the direct effect of ampelopsin on ovarian cancer
cell migration and invasion, and the underling mechanisms
have not yet been clearly established. The aim of the present
study was to investigate the influence of ampelopsin on the
migration and invasion of ovarian cancer. Proliferation and
viability of the ovarian cancer cells were detected by MTT
assay. Migration and invasion of the cells were detected,
respectively, by scratch wound healing assay and Transwell
assay. The expression levels of epithelial-to-mesenchymal
transition (EMT) markers were detected at the protein level
after stimulation with ampelopsin. Then, the expression
levels of NF-κB and p-IκBα were detected with western blot
analysis. Meanwhile, an inhibitor of NF-κB was used to investigate
the effect of ampelopsin. Finally, the expression of Snail
was also detected. Proliferation, migration and invasion of the
A2780 cells were all inhibited following the application of
ampelopsin. Ampelopsin upregulated E-cadherin and downregulated
N-cadherin and vimentin in a concentration- and
time-dependent manner. Ampelopsin also exerted its ability
to suppress the nuclear translocation of the NF-κB pathway.
Administration of the inhibitor BAY11‑7082 confirmed the
roles of NF-κB in the expression of EMT markers and its transcription
factor. These results demonstrated that ampelopsin
inhibited EMT and reduced the invasion of ovarian cancer
cells via the NF-κB/Snail pathway.
Funding
This study was supported by the Natural Science Foundation
of Shandong Province (no. 2012ZRE27087).