Research Article

Forkhead box protein O1 mediates apoptosis in a cancer cervical cell line treated with the antitumor agent tumor necrosis factor-α

Published: July 06, 2015
Genet. Mol. Res. 14 (3) : 7446-7454 DOI: 10.4238/2015.July.3.20

Abstract

Tumor necrosis factor-α (TNF-α) is an important pro-apoptotic cytokine, which performs a broad range of immune and inflammatory functions in several vital processes. TNF-α-induced apoptosis has been confirmed, however, relatively little is known regarding the role of forkhead box class-O 1 (FOXO1) in mediating TNF-α-induced apoptosis in cervical cancer. In our study, we used the well-characterized cervical cancer cell line C-33A to investigate the role of FOXO1. The results showed that the antitumor agent TNF-α increased the expression level of FOXO1 (P < 0.05) and enhanced its transcriptional activity (P < 0.05). Furthermore, knockdown of FOXO1 repressed TNF-α-induced apoptosis and caspase-3, 8, and 9 expressions (P < 0.05). Collectively, these findings suggest that TNF-α upregulated the transcriptional factor FOXO1, leading to an increased expression of apoptotic gene, which leads to an increase in apoptosis.

Tumor necrosis factor-α (TNF-α) is an important pro-apoptotic cytokine, which performs a broad range of immune and inflammatory functions in several vital processes. TNF-α-induced apoptosis has been confirmed, however, relatively little is known regarding the role of forkhead box class-O 1 (FOXO1) in mediating TNF-α-induced apoptosis in cervical cancer. In our study, we used the well-characterized cervical cancer cell line C-33A to investigate the role of FOXO1. The results showed that the antitumor agent TNF-α increased the expression level of FOXO1 (P < 0.05) and enhanced its transcriptional activity (P < 0.05). Furthermore, knockdown of FOXO1 repressed TNF-α-induced apoptosis and caspase-3, 8, and 9 expressions (P < 0.05). Collectively, these findings suggest that TNF-α upregulated the transcriptional factor FOXO1, leading to an increased expression of apoptotic gene, which leads to an increase in apoptosis.