Open AccessGene Expression Profiling of Human Myeloid Leukemic MV4-11 Cells Treated with 5-Aza-2’-deoxycytidine
Author(s) -
Kyu-Tae Kim,
David Mossman,
Donald Small,
Rodney J. Scott
Publication year - 2012
Publication title -
journal of cancer therapy
Language(s) - English
Resource type - Journals
eISSN - 2151-1942
pISSN - 2151-1934
DOI - 10.4236/jct.2012.33025
Subject(s) - gene , myeloid leukemia , biology , gene expression profiling , microbiology and biotechnology , cancer research , microarray , gene expression , methyltransferase , phenotype , dna demethylation , microarray analysis techniques , leukemia , dna methylation , methylation , genetics
The pyrimidine analog, 5-aza-2’-deoxycytidine (5-aza-dC) is a DNA methyltransferase inhibitor that triggers DNA demethylation leading to the reactivation of epigenetically silenced tumor suppressor genes. To understand the shift in gene expression which mediates the beneficial 5-aza-dC effects in leukemia, we have treated human myeloid derived leukemic cells with 5-aza-dC. Target genes were identified first in MV4-11 cells using a genome-wide gene expression profiling assay to detect differences in treated and untreated cells. From this analysis six genes were identified (HOXA4, HOXD4, HOXA8, HOXD12, CD9 and RGS2) as being significantly different expressed after treatment. To validate microarray data, we performed quantitative PCR on these genes from multiple leukemic cells. The results suggest that these genes are epigenetically regulated indicating that dysregulation of HOXA4, HOXD4, HOXA8, HOXD12, CD9 and RGS2 expression may play an important role in establishing the malignant phenotype in AML