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KMID : 1140220130180030264
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대한암예방학회지
2013 Volume.18 No. 3 p.264 ~ p.270
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Quercetin Regulates Sestrin 2-AMPK-mTOR Signaling Pathway and Induces Apoptosis via Increased Intracellular ROS in HCT116 Colon Cancer Cells
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Kim Guen-Tae
Lee Se-Hee
Kim Young-Min
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Abstract
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Background: The suppression of abnormal cell proliferation is therapeutic strategies for the treatment of cancer. In this study, we investigated the regulatory mechanism of quercetin-induced apoptosis through regulation of Sestrin 2 and AMPK signaling pathway.
Methods: After treatment of quercetin to colon cancer cells, intracellular ROS was detected using by DCFH-DA. To examine how quercetin and H2O2 induced apoptosis, we analyzed the change of Sestrin 2, p53 expression and p-AMPKα1, p-mTOR levels by Western blotting. To evaluate the effect of intracellular ROS generated by quercetin on colon cancer cells, NAC, anti-oxidative agent, was co-treated.
Results: Quercetin increased apoptotic cell death though generating intracellular reactive oxygen species (ROS), and it was responsible for Sestrin 2 expression. Increased Sestrin 2 expression was accompanied by AMPK activation. Interestingly, mTOR activity by Sestirn 2 expression was dependent on AMPK phosphorylation. On the other hand, the expression of Sestrin 2 by quercetin-generated intracellular ROS was independent of p53.
Conclusions: We suggested that quercetin-induced apoptosis involved Sestrin 2/AMPK/mTOR pathway, which was regulated by increased intracellular ROS by quercetin.
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KEYWORD
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Quercetin, ROS, Sestrin2, AMPK, p53
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