Inhibitory Effect and Mechanisms of an Anthocyanins- and Anthocyanidins-Rich Extract from Purple-Shoot Tea on Colorectal Carcinoma Cell Proliferation
Author(s) -
ChihPing Hsu,
Yi-Ting Shih,
BorRu Lin,
Chui-Feng Chiu,
ChihCheng Lin
Publication year - 2012
Publication title -
journal of agricultural and food chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.203
H-Index - 297
eISSN - 1520-5118
pISSN - 0021-8561
DOI - 10.1021/jf204619n
Subject(s) - anthocyanidins , apoptosis , cell cycle , chemistry , cyclin d1 , cell growth , colorectal cancer , delphinidin , cyclin b1 , cell cycle checkpoint , cancer research , anthocyanin , biochemistry , cyclin dependent kinase 1 , biology , cyanidin , flavonoid , cancer , medicine , antioxidant , food science
One newly bred variety of tea cultivar, purple-shoot tea, was selected to evaluate its antiproliferative effects on colorectal carcinoma cells, as well as normal colon cells. The phytochemicals and identified catechins of purple-shoot tea extract (PTE) were significantly higher than that of ordinary tea, especially the anthocyanins (surpassed by 135-fold) and anthocyanidins (surpassed by 3.5-fold). PTE inhibited the proliferation of COLO 320DM (IC(50) = 64.9 μg/mL) and HT-29 (IC(50) = 55.2 μg/mL) by blocking cell cycle progression during the G(0)/G(1) phase and inducing apoptotic death. Western blotting indicated that PTE induced cell cycle arrest by reducing the expression of cyclin E and cyclin D1 in COLO 320DM and the upregulation of p21 and p27 cyclin-dependent kinase inhibitors in HT-29. Two cells treated with PTE also indicated the cleavage of PARP, activation of caspase 3, and an increased Bax/Bcl-2 ratio. Our results showed that PTE is a potential novel dietary agent for colorectal cancer chemoprevention.
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