Astaxanthin Inhibits Proliferation of Human Gastric Cancer Cell Lines by Interrupting Cell Cycle Progression.
- Author:
Jung Ha KIM
1
;
Jong Jae PARK
;
Beom Jae LEE
;
Moon Kyung JOO
;
Hoon Jai CHUN
;
Sang Woo LEE
;
Young Tae BAK
Author Information
1. Division of Gastroenterology, Department of Internal Medicine, Korea University Guro Hospital, Korea University College of Medicine, Seoul, Korea. gi7pjj@yahoo.co.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Astaxanthin;
Human gastric adenocarcinoma;
Proliferation;
Extracellular signal-regulated kinase;
p27(kip-1)
- MeSH:
Adenocarcinoma;
Cell Cycle*;
Cell Line*;
Cell Survival;
Humans*;
Immunoblotting;
Phosphorylation;
Phosphotransferases;
S Phase;
Stomach Neoplasms*
- From:Gut and Liver
2016;10(3):369-374
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/AIMS: Astaxanthin is a carotenoid pigment that has antioxidant, antitumoral, and anti-inflammatory properties. In this in vitro study, we investigated the mechanism of anticancer effects of astaxanthin in gastric carcinoma cell lines. METHODS: The human gastric adenocarcinoma cell lines AGS, KATO-III, MKN-45, and SNU-1 were treated with various concentrations of astaxanthin. A cell viability test, cell cycle analysis, and immunoblotting were performed. RESULTS: The viability of each cancer cell line was suppressed by astaxanthin in a dose-dependent manner with significantly decreased proliferation in KATO-III and SNU-1 cells. Astaxanthin increased the number of cells in the G0/G1 phase but reduced the proportion of S phase KATO-III and SNU-1 cells. Phosphorylated extracellular signal-regulated kinase (ERK) was decreased in an inverse dose-dependent correlation with astaxanthin concentration, and the expression of p27(kip-1) increased the KATO-III and SNU-1 cell lines in an astaxanthin dose-dependent manner. CONCLUSIONS: Astaxanthin inhibits proliferation by interrupting cell cycle progression in KATO-III and SNU-1 gastric cancer cells. This may be caused by the inhibition of the phosphorylation of ERK and the enhanced expression of p27(kip-1).
