(PO02-03-22) Lutein Induces Apoptosis of Gastric Cancer Cells by Producing Reactive Oxygen Species via NADPH Oxidase Activation

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Presenting Author(s)

JE

Juwon Eom, B.S.
– 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):

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

Objectives: Apoptosis is well known for its relationship with cancer. Disruption of apoptosis leads to tumor progression, and many cytotoxic anticancer agents induce apoptosis. As a class of phytochemicals, carotenoids are fat-soluble pigments that are abundant in fruits and vegetables and have health-promoting properties, including cancer prevention effects. The anticancer effects of carotenoids are related to their pro-oxidant activities. Lutein is a type of vitamin called a carotenoid. A recent study showed that lutein inhibits the growth of breast cancer cells. The present study was purposed to determine whether lutein induces apoptosis of gastric cancer cells through reactive oxygen species (ROS)-mediated mechanism.

Methods: Human gastric cancer cell line, AGS was treated with lutein. Cell viability was determined by counting the number of viable cells. The protein levels of Bax, Bcl-2, active caspase-3 were examined by western blot analysis. DNA fragmentation was determined by Cell Death Detection ELISA. DCF-DA fluorescence technique was used to quantify the intracellular ROS level. NADPH oxidase activity was measured by lucigenin assay. Colony formation assay was performed and colonies were counted.

Results: Lutein decreased cell viability in a dose-dependent manner. Colony formation was also inhibited by lutein. Lutein increased Bax/Bcl-2 ratio, caspase-3 activity, and DNA fragmentation. The intracellular ROS level and NADPH oxidase activity were increased. The decrease in cell viability by lutein was reversed by ML171 (NADPH oxidase 1 specific inhibitor) and N‑acetyl cysteine (NAC; antioxidant).

Conclusions: Lutein induce apoptosis of gastric cancer cells by increasing NADPH oxidase-mediated ROS production.

Funding Sources: No funding sources