The effect of Longan seed polyphenols on colorectal carcinoma cells

• Published in: European journal of clinical investigation 2010-08, Vol.40 (8), p.713-721
• Main Authors: Chung, Yuan-Chiang, Lin, Chih-Cheng, Chou, Chih-Chung, Hsu, Chih-Ping
• Format: Article
• Language: English
• Subjects: Apoptosis; Apoptosis - drug effects; Biological and medical sciences; Blotting, Western; Carcinoma - drug therapy; Carcinoma - pathology; Caspase 3 - metabolism; cell cycle; Cell Line, Tumor; Cell Proliferation - drug effects; colorectal carcinoma; Colorectal Neoplasms - drug therapy; Colorectal Neoplasms - pathology; Cyclin A - metabolism; Cyclin D1 - metabolism; Flavonoids - analysis; Flavonoids - pharmacology; Flow Cytometry; Gastroenterology. Liver. Pancreas. Abdomen; General aspects; Humans; Longan seed polyphenols; Medical sciences; Phenols - pharmacology; Plant Extracts - chemistry; Plant Extracts - pharmacology; Polyphenols; S Phase - drug effects; Sapindaceae - chemistry; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Tumors
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1111/j.1365-2362.2010.02322.x

Eur J Clin Invest 2010; 40 (8): 713–721 Background  Polyphenol‐rich longan seed extract (LSP) is a free radical scavenger and antioxidant. However, the effect of LSP on the growth of human colorectal carcinoma cells (CRC) has not yet been evaluated. Materials and methods  Polyphenols of longan seeds were extracted and measured by colorimetry. Four CRC cell lines (Colo 320DM, SW480, HT‐29 and LoVo) were treated with LSP and assessed for viability by trypan blue exclusion, for cell cycle distribution by flow cytometry, for apoptosis by annexin V labelling and for changes in the levels of proteins involved in cell cycle control or apoptosis by immunoblotting. Results  Total phenol content of LSP was 695 mg g−1 and total flavonoids were 150 mg g−1. LSP inhibited the proliferation (25 μg mL−1–200 μg mL−1) of Colo 320DM, SW480 and HT‐29, but not LoVo. LSP inhibited the proliferation by blocking cell cycle progression during the DNA synthesis phase and inducing apoptotic death. Western blotting indicated that LSP blocks the S phase, reducing the expression of cyclin A and cyclin D1. Colo 320DM and SW480 treated with LSP also showed the activation of caspase 3 and increased Bax : Bcl‐2 ratio. Conclusion  LSP induces S phase arrest of the cell cycle and apoptotic death in three CRC cell lines. The results indicate that LSP is a potential novel chemoprevention and treatment agent for colorectal cancer.