(PO23-13-22) Astaxanthin Inhibits Helicobacter pylori-Induced MMPs Expression and Cell Invasion by Suppressing PI3K-AKT-mTOR Pathways in AGS Cells

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Presenting Author(s)

JL

Jimin Lee, B.S
– Graduate student, Yonsei University, seoul, Seoul-t'ukpyolsi, Republic of Korea

Co-Author(s)

HK

Hyeyoung Kim, Ph.D.
– Professor, Yonsei University, Seoul, Seoul-t'ukpyolsi, Republic of Korea
JL

Joo Weon Lim, Ph.D.
– Research Professor, Yonsei University, Seoul, Seoul-t'ukpyolsi, Republic of Korea

Disclosure(s):

Jimin Lee, B.S: No relevant financial relationship(s) with ineligible companies to disclose.

Objectives: Matrix metalloproteinases (MMPs) are members of the metzincin group of proteases which can degrade various components of extracellular matrix components (ECM). ECM degradation by MMPs not only enhances tumor invasion but also affects tumor cell behavior and leads to cancer progression. Resent reports demonstrated that PI3K-AKT-mTOR signaling pathways are involved in expression of MMPs. Especially when it comes to gastric cancer, H. pylori infection promotes the invasion and metastasis of tumor cells by reactive oxygen species (ROS). Astaxanthin, a xanthophyll carotenoid, has been well known for its strong antioxidant and anticancer properties. Thus, the present study was aimed to investigate the inhibitory effects and mechanisms of astaxanthin on H. pylori-induced MMPs expression and cell invasion in human gastric epithelial cells.

Methods: Human gastric epithelial cell lines,AGS were used. AGS cells were pre-treated with astaxanthin for 3 hours prior to H. pylori (cag A positive NCTC 11637 strains) infection at bacterium/cell ratio of 50:1 and cultured for 24 hours in the presence of H. pylori. mRNA expression and protein levels of MMP-7 and 10 was measured by real time PCR and Western blot analysis, respectively. Intracellular ROS levels were determined using DCF-DA. Invasive cell phenotype was measured using invasion assay.

Results: Astaxanthin inhibited expression of MMP-7&10. Intracellular ROS production and cell invasion induced by H. pylori was inhibited by astaxanthin. In addition, H. pylori-induced activation of PI3K-AKT-mTOR was inhibited by astaxanthin.

Conclusions: Astaxanthin exerts an inhibitory effect on H. pylori-induced MMPs expression and cell invasion by suppression of ROS production and PI3K-AKT-mTOR signaling pathway in gastric epithelial cells. Thus astaxanthin may hold promise for clinical cancer therapy.

Funding Sources: No funding sources