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Evidence for Anti‐carcinogenic effect of Synthetic flavanone derivatives in human breast cancer cells
Author(s) -
Choi Eun Jeong,
Lee Jae In,
Kim GunHee
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1346-a
Subject(s) - flavanone , apoptosis , chemistry , cell growth , cell cycle checkpoint , cell cycle , cytochrome c , cyclin d1 , cancer cell , cyclin a , carcinogen , cancer research , microbiology and biotechnology , cancer , biochemistry , biology , medicine , antioxidant , flavonoid
We investigated the effects of synthetic flavanone derivatives on the proliferation and apoptosis of human breast cancer cells and explored the mechanism behind these effects. When cells were treated with synthetic flavanone derivatives in concentrations ranging from 1 to 200 uM for 48 h, cell growth decreased at concentrations above 50 uM in both MCF‐7 and MDA‐MB‐453 cells. 4′‐chloroflavanone is more potent than flavanone among the synthetic flavanone derivatives. Exposure to 4′‐chloroflavanone at 50 uM for 48 h caused cell cycle arrest in both cells. In addition, when 4′‐chloroflavanone caused G1/S phase arrest, a decrease in CDK4 and cyclin D together with an increase in p21 Cip1 was observed in the cells. The p21 Cip1 is a downstream target of p53 that may be affected by the activation of p53 by 4′‐chloroflavanone. These results indicate that the activation of p53 played some role in 4′‐chloroflavanone‐induced cell cycle arrest of human breast cancer cells. 4′‐chloroflavanone increased cytochrome c expression and decreased the expression of caspase‐3, but did not change the expression of Bcl‐2 and Bax. Activation of cytochrome c and it downstream target, caspase‐3, is suggested to be an important inducer of the apoptosis process by 4′‐chloroflavanone. 4′‐chloroflavanone inhibits cell proliferation through G1/S phase disruption and may induce apoptosis.