Low concentration of MNK1 inhibitor CGP57380 inhibits the proliferation of human lung adenocarcinoma A549 cells and induces their apoptosis
10.3781/j.issn.1000-7431.2013.10.005
- Author:
Xiao-Yuan SU
1
Author Information
1. Hub Laboratory
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Cell proliferation;
Eukaryotic initiation factor-4E;
Lung neoplasms;
Mitogen-activated protein kinases;
Protease inhititors, CGP57380;
Receptor-interacting protein serine-threonine kinases
- From:
Tumor
2013;33(10):873-878
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To observe the effects of low concentration of CGP57380, an inhibitor of mitogen-activated protein kinase-interacting kinase 1 (MNK1) on the proliferation and apoptosis of human lung adenocarcinoma A549 cells. Methods: A549 cells were treated with low concentrations (1-4 μmol/L) CGP57380 for 24-72 hours, then the cell proliferation was assessed by MTT assay, and the apoptosis and cell cycle distribution were detected by flow cytometry. The expression levels of phosphorylated MNK1 (p-MNK1) and phosphorylated human eukaryotic translation initiation factor 4E (p-eIF4E) proteins in A549 cells treated with 1 μmol/L CGP57380 for 48 hours were examined by Western blotting. Results: Comparing to the control, the proliferation of A549 cells was inhibited after treatment with different concentrations of CGP57380 for 48 hours (all P < 0.05). A549 cells treated with 2-4 μmol/L CGP57380 for 72 hours were induced G2/M cell cycle arrest (both P < 0.05). CGP57380 at different concentrations could induce dose-dependent apoptosis in A549 cells. The expression levels of p-MNK1 and p-eIF4E were significantly lower in A549 cells treated with 1 μmol/L CGP57380 than those in the control (P < 0.05). Conclusion: Low concentration of CGP57380 can inhibit the proliferation of human lung adenocarcinoma A549 cells and induce their apoptosis, implying that MNK1 gene may be a candidate target for the treatment of lung cancer. Copyright © 2013 by TUMOR.
