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KMID : 1140220190240030192
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2019 Volume.24 No. 3 p.192 ~ p.196
¥â-carotene Inhibits Expression of c-Myc and Cyclin E in Helicobacter pylori-infected Gastric Epithelial Cells
Kim Da-Hye

Lim Joo-Weon
Kim Hye-Young
Abstract
Background: Helicobacter pylori infection is a major risk factor in the development of gastric cancer. H. pylori infection of gastric epithelial cells increases the levels of reactive oxygen species (ROS), activates oncogenes, and leads to ¥â-catenin-mediated hyper-proliferation. ¥â-Carotene reduces ROS levels, inhibits oxidant-mediated activation of inflammatory signaling and exhibits anticancer properties. The present study was carried out to determine if ¥â-carotene inhibits H. pylori-induced cell proliferation and the expression of oncogenes c-myc and cyclin E by reducing the levels of ¥â-catenin and phosphorylated glycogen synthase kinase 3¥â (p-GSK3¥â).

Methods: Gastric epithelial AGS cells were pre-treated with ¥â-carotene (5 and 10 ¥ìM) for 2 hours prior to H. pylori infection and cultured for 6 hours (for determination of the levels of p-GSK3¥â, GSK3¥â, and ¥â-catenin) and 24 hours (for determination of cell viability and protein levels of c-myc and cyclin E). Cell viability was determined by the MTT assay and protein levels were determined via western blot-based analysis.

Results: ¥â-Carotene inhibited H. pylori-induced increases in the percentage of viable cells, phosphorylated GSK3¥â (p-GSK3¥â), and the levels of ¥â-catenin, c-myc and cyclin E.

Conclusions: ¥â-Carotene inhibits H. pylori-induced hyper-proliferation of gastric epithelial cells by suppressing ¥â-catenin signaling and oncogene expression.
KEYWORD
Beta carotene, Beta catenin, Helicobacter pylori, Epithelial cells, Oncogenes
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