Publication Date:
2008-11-16
Description:
Recently, it was reported that reduced level of PU.1 expression developed acute myeloid leukemia (AML) in mice. To clarify the mechanisms of AML, first we established PU.1 knockdown K562 (K562PU.1KD) cells, that express reduced level of PU.1 by stably transfected PU.1 siRNA. Flow cytometric analysis demonstrated that among other lineage markers, expressions of myeloid CD13/CD33 markers are significantly decreased in K562PU.1KD cells compared to control cells. We next tried to identify PU.1 target genes to elucidate the mechanisms of AML. To solve this, microarray and real time PCR analyses were performed. We revealed that several genes including metallothionein (MT) s (MT-1G, MT-1A) were markedly induced in K562PU.1KD cells. MTs are a group of low-molecular weight, cysteine rich intracellular proteins. A number of studies have shown an increased expression of MTs in various human solid tumors. To verify the relevance, we established PU.1 over-expressed K562 (K562PU.1OE) cells and found the significant suppression of these genes. Furthermore, we revealed a negative correlation between PU.1 and MTs mRNA expression in 43 primary AML specimens (MT-1G; R=−0.50, p
Print ISSN:
0006-4971
Electronic ISSN:
1528-0020
Topics:
Biology
,
Medicine
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