Eukaryotic initiation factor 4E (
eIF4E) plays an important role in cap-dependent translation. The overexpression of
eIF4E gene has been found in a variety of human
malignancies. In this study, we attempted to identify the potential effects of
eIF4E and explore the possibility of
eIF4E as a therapeutic target for the treatment of human
ovarian cancer. First the activation of
eIF4E protein was detected with
m7-GTP cap binding assays in
ovarian cancer and control cells. Next, the eIF4E-shRNA expression plasmids were used to specifically inhibit
eIF4E activity in
ovarian cancer cells line A2780 and C200. The effects of knockdown
eIF4E gene on cell proliferation, migration and invasion were investigated in vitro. Moreover, the changes of cell cycle and apoptosis of
ovarian cancer cells were detected by flow cytometry. Finally, we investigated the effect of knockdown of
eIF4E on the chemosensitivity of
ovarian cancer cells to
cisplatin in vitro. Our results show there is elevated activation of
eIF4E in
ovarian cancer cells compared with normal human ovarian epithelial cell line. The results of
BrdU incorporation and FCM assay indicate that knockdown of
eIF4E efficiently suppressed cell growth and induce cell cycle arrest in G1 phase and subsequent apoptosis in
ovarian cancer cells. From Transwell assay analysis, knockdown
eIF4E significantly decrease cellular migration and invasion of
ovarian cancer cells. We also confirmed that knockdown
eIF4E could synergistically enhance the cytotoxicity effects of
cisplatin to
cancer cells and sensitized
cisplatin-resistant C200 cells in vitro. This study demonstrates that the activation of
eIF4E gene is an essential component of the malignant phenotype in
ovarian cancer, and aberration of
eIF4E expression is associated with proliferation, migration, invasion and chemosensitivity to
cisplatin in
ovarian cancer cells. Knockdown
eIF4E gene can be used as a potential therapeutic target for the treatment of human
ovarian cancer.