Potential interventional mechanism of phosphorylation of P65 and ERK proteins in proliferation of PC9 lung adenocarcinoma cells

Abstract

Objective To identify the inhibitive effect of caffeic acid phenethyl ester (CAPE) on proliferation of PC9 lung adenocarcinoma cells in vitro and detect the phosphorylation of P65/extracellular regulated protein kinase (ERK) proteins induced by transforming growth factor-β1 (TGF-β1) with/without pre-treated by CAPE in PC9 cells. Methods The PC9 lung adenocarcinoma cells were treated with DMSO (as a negative control group) and CAPE, the viability of PC9 cells was evaluated by detecting the cell bioactivity using Celltiter BLUE in each group after 24, 48, 72 hours.Furthermore, the phosphorylation of P65 and ERK 1/2 proteins was induced by TGF-β1 in PC9 cells.As an intervention group, PC9 cells were pre-treated with CAPE for 30 minutes before administration with TGF-β1.Subsequently, the protein levels of phospho-P65 and phospho-ERK1/2 were measured by Western blot method to investigate the potential interventional effect of CAPE on the activation of nuclear factor-kappa B (NF-κB) pathway and ERK pathway. Results CAPE attenuated the viabilty of PC9 lung adenocarcinoma cells and inhibited cell proliferation.After treated with TGF-β1, the phosphorylation of P65 and ERK 1/2 was increased.CAPE inhibited the phosphorylation of P65 induced by TGF-β1 in vitro.However, CAPE did not inhibite the phosphorylation of ERK1/2. Conclusions CAPE can provide a new therapeutic approach for lung carcinoma.And its underlying mechanism may be related to the potential interventional effect on NF-κB pathway.However, the effect on ERK pathway remains unfounded. Key words: Adenocarcinoma of lung; Proliferation; Phosphorylation; Transforming growth factor-β1