Abstract Title:

[Effect of lycopene on the proliferation of MCF-7 and MDA-MB-231 cells].

Abstract Source:

Sichuan Da Xue Xue Bao Yi Xue Ban. 2007 Nov;38(6):958-60, 976. PMID: 18095595

Abstract Author(s):

Ai-hong Wang, Li-shi Zhang

Article Affiliation:

Department of Nutrition and Food Hygiene, West China School of Public Health, Sichuan University, Chengdu 610041, China.

Abstract:

OBJECTIVE: To test the effect of lycopene on the proliferation and apoptosis of the estrogen receptor(ER)-positive MCF-7 and ER-negative MDA-MB-231 human breast cancer cell lines. METHODS: The cell proliferation was analyzed by the MTT and the H3-TdR incorporation. The effect of lycopene on the cell cycle and apoptosis of the synchronized cells was observed through flow cytometry. RESULTS: Lycopene inhibited the growth and DNA synthesis of both ER-positive MCF-7 and ER-negative MDA-MB-231 cells in a dose-dependent pattern. The maximum inhibition effect appeared after 4 days of exposure to lycopene, with an inhibition rate of 52.6% and 61.9% for the MCF-7 and MDA-MB-231 cells respectively. The flow cytometry analysis found more cells in the G0/G1 phase and less cells in the S and G2/M phase after 24 hours of exposure to lycopene. Lycopene induced apoptosis for the MDA-MB-231 cells, but not for the MCF-7 cells. CONCLUSION: Lycopene inhibits the growth of ER-positive MCF-7 cells through the inhibition of the cell cycle progression. The inhibition of ER- negative MDA-MB-231 cells by lycopene is associated not only with the G1 phase cell cycle-arrest but also the induction of apoptosis.

Study Type : In Vitro Study

Print Options


Key Research Topics

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2024 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.