Abstract Title:

HDAC1 expression and effect of curcumin on proliferation of Raji cells.

Abstract Source:

J Huazhong Univ Sci Technolog Med Sci. 2006;26(2):199-201, 210. PMID: 16850746

Abstract Author(s):

Qing Wu, Yan Chen, Xinggang Li

Article Affiliation:

Institute of Hematology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Abstract:

Histone deacetylase (HDAC1) has a high expression in many cancer cells and curcumin can inhibit the growth of cancer cells. This paper was designed to investigate the expression of HDAC1 of Raji cells and the effect of curcumin on their proliferation and apoptosis. Raji cells were treated with 3.125-50 micromol/L curcumin for 8-48 h and the growth inhibition rates of Raji cells were measured by MTT. The expression of HDAC1 on Raji cells were examined by mRNA, Western blot at 24 h various concertrations (1.6-50 micromol/L). Curcumin could selectively inhibit the proliferation of Raji cells in a dose- and time-dependent manner, with the inhibition rate being 52.47 %-82.18 % (P<0.01). The up-regulation of HDAC1 expression was observed within 24 h after the treatment with curcumin as shown by RT-PCR and Western blot. With the increase of concentration, the expression was down-regulated in a dose- dependent manner. It is concluded that the expression of HDAC1 plays an important role in the proliferation and apoptosis of Raji cells and curcumin can inhibit the growth of Raji cells at various concentrations and promote the apoptosis of Raji cells.

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.