Naringenin-Mediated ATF3 Expression Contributes to Apoptosis in Human Colon Cancer.
10.4062/biomolther.2015.109
- Author:
Hun Min SONG
1
;
Gwang Hun PARK
;
Hyun Ji EO
;
Jin Boo JEONG
Author Information
1. Department of Bioresource Sciences, Andong National University, Andong 760749, Republic of Korea. jjb0403@anu.ac.kr
- Publication Type:Original Article
- Keywords:
Naringenin;
Activating transcription factor 3;
Cancer chemoprevention;
Human colon cancer
- MeSH:
Activating Transcription Factor 3;
Apoptosis*;
Cell Survival;
Citrus paradisi;
Colon*;
Colonic Neoplasms*;
Flavonoids;
Humans*;
Luciferases;
RNA, Messenger;
Transcriptional Activation
- From:Biomolecules & Therapeutics
2016;24(2):140-146
- CountryRepublic of Korea
- Language:English
-
Abstract:
Naringenin (NAR) as one of the flavonoids observed in grapefruit has been reported to exhibit an anti-cancer activity. Activating transcription factor 3 (ATF3) is associated with apoptosis in human colon cancer cells. This study was performed to investigate the molecular mechanism by which NAR stimulates ATF3 expression and apoptosis in human colon cancer cells. NAR reduced the cell viability and induced an apoptosis in human colon cancer cells. ATF3 overexpression increased NAR-mediated cleaved PARP, while ATF3 knockdown attenuated the cleavage of PARP by NAR. NAR increased ATF3 expression in both protein and mRNA level, and increased the luciferase activity of ATF3 promoter in a dose-dependent manner. The responsible region for ATF3 transcriptional activation by NAR is located between -317 and -148 of ATF3 promoter. p38 inhibition blocked NAR-mediated ATF3 expression, its promoter activation and apoptosis. The results suggest that NAR induces apoptosis through p38-dependent ATF3 activation in human colon cancer cells.
