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Journal of Cancer Prevention

Original Article

Cancer prevention research 2012; 17(3): 244-250

Published online September 30, 2012

© Korean Society of Cancer Prevention

Quercetin of Plants Extracts Regulates Sestrin2 and Induces Apoptosis in HT-29 Colon Cancer Cells

Se Hee Lee1, Da-Woon Jeong1, Guen Tae Kim1, Song Yi Park1, Seon Young Kim1, Ock Jin Park2 and Young Min Kim1


Quercetin is an important anti-cancer flavonoid, present in various vegetable, fruits and etc. It has been shown to inhibit cell proliferation in several cancer types. And this substance can generate ROS to cause free radical-induced apoptosis. Sestrin2, a stress-responsive gene, plays a role in the regulation of autophagy and tumor suppressive metabolism through modulation of p-AMPK-p-mTOR signaling pathway. DNA damage and oxidative stress, such as ROS conditions, stimulated sestrin2 and overexpression of sestrin2 led to increase p-AMPK and suppress p-mTOR pathway. In this study, we have explored the anti-proliferatory effects of quercetin in HT-29 colon cancer cells through sestrin2, p-AMPK and p-mTOR and focused on the regulation effects of sestrin2 by treatment of quercetin. We revealed that quercetin inhibits cell proliferation in HT-29 cells and determined that quercetin modulates protein levels of sestrin2, p-AMPK and p-mTOR. Treatment of quercetin resulted in expression of the sestrin2. These regulations affect activation of p-AMPK and decrease of p-mTOR levels. Blocking AMPK activity using Compound C showed that quercetin-inhibited p-mTOR should be stimulated by p-AMPK. These results indicated that quercetin controls sestrin2, but regulation of p-mTOR needs to be triggered by p-AMPK. Thus the p-AMPK-p-mTOR signaling pathway is regulated by quercetin-activated discovery of sestrin2. (Cancer Prev Res 17, 0-250, 2012)

Keywords: Sestrin2, p-AMPK, p-mTOR, Quercetin, Apoptosis

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