Flavanones inhibit the clonogenicity of HCT116 cololectal cancer cells

被引:27
|
作者
Woo, Yoonkyung [1 ]
Shin, Soon Young [2 ]
Hyun, Jiye [1 ]
Lee, Sung Dae [3 ]
Lee, Young Han [2 ]
Lim, Yoongho [1 ]
机构
[1] Konkuk Univ, Div Biosci & Biotechnol, BMIC, MoleNBio, Seoul 143701, South Korea
[2] Konkuk Univ, RCTC, SMART Inst Adv Biomed Sci, Dept Biomed Sci & Technol, Seoul 143701, South Korea
[3] RDA, Natl Inst Anim Sci, Swine Sci Div, Cheonan 330801, South Korea
关键词
flavanone; colorectal cancer; HCT116; cell; quantitatively SAR; clonogenicity; RHUS-VERNICIFLUA; COLON-CANCER; GENE; PINOCEMBRIN; DERIVATIVES; NARINGENIN; EXPRESSION; FLAVONOIDS; MECHANISM; THERAPY;
D O I
10.3892/ijmm.2011.857
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Naringen in has been shown to display various biological effects such as antioxidant, anticancer, anti-inflammatory, and antiviral activities. Taxifolin inhibits the production of lipopolysaccharide-induced prostaglandin E, and fustin suppresses the activity of acetylcholinesterase. They all belong to flavanone which is a class of flavonoids with a C6-C3-C6 skeleton. Since the anticancer activities of flavanone derivatives have rarely been reported, we examined the effects of 26 flavanone derivatives on HCT116 colorectal cancer cells. Our results suggest that flavanone derivatives control the expression of cell cycle regulatory proteins, which blocks G1 cell cycle progression and inhibits the clonogenicity of HCT116 cells. In addition, in order to design flavanone derivatives that show better anticancer activity, structure-activity relationships were examined.
引用
收藏
页码:403 / 408
页数:6
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