Expression profiling of stem cell signaling alters with spheroid formation in CD133 high /CD44 high prostate cancer stem cells
Cancer stem cells (CSC) isolated from multiple tumor types differentiate and when cultured in serum; however, the factors responsible for their differentiation have not yet been identified. The first aim of the present study was to identify CD133 /CD44 DU145 prostate CSCs and compare their profiles...
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Veröffentlicht in: | Oncology letters 2014-06, Vol.7 (6), p.2103 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Cancer stem cells (CSC) isolated from multiple tumor types differentiate
and
when cultured in serum; however, the factors responsible for their differentiation have not yet been identified. The first aim of the present study was to identify CD133
/CD44
DU145 prostate CSCs and compare their profiles with non-CSCs as bulk counterparts of the population. Subsequently, the two populations continued to be three-dimensional multicellular spheroids. Differentiation was then investigated with stem cell-related genomic characteristics. Polymerase chain reaction array analyses of cell cycle regulation, embryonic and mesenchymal cell lineage-related markers, and telomerase reverse transcriptase (
) and
signaling were performed. Immunohistochemistry of
,
,
,
,
,
,
,
,
and
were determined in CSC and non-CSC monolayer and spheroid subcultures. Significant gene alterations were observed in the CD133
/CD44
population when cultured as a monolayer and continued as spheroid. In this group, marked gene upregulation was determined in
,
and
,
and
were respectively upregulated genes in the Notch signaling pathway. According to immunoreactivity, the staining density of
,
,
and
increased significantly in CSC spheroids. Isolated CSCs alter their cellular characterization over the course of time and exhibit a differentiation profile while maintaining their former surface antigens at a level of transcription or translation. The current study suggested that this differentiation process may be a mechanism responsible for the malignant process and tumor growth. |
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ISSN: | 1792-1074 |