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Molecular and cellular characterization of ABCG2 in the prostate
被引:48
|作者:
Pascal L.E.
[1
,2
]
Oudes A.J.
[1
,2
]
Petersen T.W.
[2
]
Goo Y.A.
[1
,2
]
Walashek L.S.
[1
,2
]
True L.D.
[3
]
Liu A.Y.
[1
,2
]
机构:
[1] Department of Urology, Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle
[2] Institute for Systems Biology, Seattle
[3] Department of Pathology, University of Washington, Seattle
来源:
关键词:
Side Population;
Hank Balance Salt Solution;
Side Population Cell;
Prostate Stem Cell Antigen;
Basal Epithelium;
D O I:
10.1186/1471-2490-7-6
中图分类号:
学科分类号:
摘要:
Background. Identification and characterization of the prostate stem cell is important for understanding normal prostate development and carcinogenesis. The flow cytometry-based side population (SP) technique has been developed to isolate putative adult stem cells in several human tissue types including the prostate. This phenotype is mainly mediated by the ATP-binding cassette membrane transporter ABCG2. Methods. Immunolocalization of ABCG2 was performed on normal prostate tissue obtained from radical prostatectomies. Normal human prostate SP cells and ABCG2(+ )cells were isolated and gene expression was determined with DNA array analysis and RT-PCR. Endothelial cells were removed by pre-sorting with CD31. Results. ABCG2 positive cells were localized to the prostate basal epithelium and endothelium. ABCG2(+ )cells in the basal epithelium constituted less than 1% of the total basal cell population. SP cells constituted 0.5-3% of the total epithelial fraction. The SP transcriptome was essentially the same as ABCG2(+ )and both populations expressed genes indicative of a stem cell phenotype, however, the cells also expressed many genes in common with endothelial cells. Conclusion. These results provide gene expression profiles for the prostate SP and ABCG2(+ )cells that will be critical for studying normal development and carcinogenesis, in particular as related to the cancer stem cell concept. © 2007 Pascal et al; licensee BioMed Central Ltd.
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