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In addition, HSP27 overexpression blocked the effects of COE on cell invasion and migration.
In order to measure effects of COE on degradation of HSP27 protein, cells were treated with the proteasome inhibitor MG132.
The effects of COE on the upregulation of E-cadherin and downregulation of N-cadherin and Vimentin were also blocked by HSP27 overexpression.
To further confirm the effects of COE on TGF-β1-induced EMT, we examined the effect of COE on expression of EMT markers by western blot assay.
In this study, we investigated the effects of COE on transforming growth factor β1 (TGF-β1) induced EMT in vitro and tumor metastasis in vivo and explored the underlying molecular mechanism.
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Moreover, overexpression of HSP27 weakens the inhibitory effect of COE on EMT, suggesting that inhibition of HSP27 is a primary event in the anti-metastatic activity of COE.
First, the effect of COE on cell viability with the MTT assay was examined at 24 h.
We investigated the effect of COE on IL-1β and TNF-α combination-induced FLS invasion as well as MMP expression and explored upstream signal transduction.
As shown in Figure 1(A), this experiment was undertaken to examine the cytotoxic effect of COE on human RA-FLSs.
As shown in Figure 4E, the overexpression of HSP27 decreased the inhibitory effect of COE on the nuclear translocation of NF-κB p65 and Snail, as well as the phosphorylation of IκBα.
To more fully investigate the effect of COE on TGF-β1 stimulated EMT process, SGC-7901 cells were incubated with or without COE (5, 10 and 20 μg/mL) for 1 h followed by treatment with 10 ng/mL TGF-β1 for 24 h.
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