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

HT-29 대장암 세포에서 식물추출물 쿼세틴에 의한 Sestrin2의 조절과 Apoptosis 유도에 관한 연구

  • Lee, Se Hee (Department of Biological Sciences and Biotechnology, College of Life Science and Nano Technology, Hannam University) ;
  • Jeong, Da-Woon (Department of Biological Sciences and Biotechnology, College of Life Science and Nano Technology, Hannam University) ;
  • Kim, Guen Tae (Department of Biological Sciences and Biotechnology, College of Life Science and Nano Technology, Hannam University) ;
  • Park, Song Yi (Department of Biological Sciences and Biotechnology, College of Life Science and Nano Technology, Hannam University) ;
  • Kim, Seon Young (Department of Biological Sciences and Biotechnology, College of Life Science and Nano Technology, Hannam University) ;
  • Park, Ock Jin (Department of Food and Nutrition, College of Life Science and Nano Technology, Hannam University) ;
  • Kim, Young Min (Department of Biological Sciences and Biotechnology, College of Life Science and Nano Technology, Hannam University)
  • 이세희 (한남대학교 생명나노과학대학 생명시스템과학과) ;
  • 정다운 (한남대학교 생명나노과학대학 생명시스템과학과) ;
  • 김근태 (한남대학교 생명나노과학대학 생명시스템과학과) ;
  • 박송이 (한남대학교 생명나노과학대학 생명시스템과학과) ;
  • 김선영 (한남대학교 생명나노과학대학 생명시스템과학과) ;
  • 박옥진 (한남대학교 생명나노과학대학 식품영양학과) ;
  • 김영민 (한남대학교 생명나노과학대학 생명시스템과학과)
  • Published : 2012.09.30

Abstract

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.

Keywords

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