Expression of heat shock protein 70 and NKG2D ligands in acute myeloid leukemia cell lines
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Leukemia, Myeloid, Acute metabolism MeSH
- Cell Membrane metabolism MeSH
- Killer Cells, Natural cytology MeSH
- Adult MeSH
- HL-60 Cells MeSH
- Cohort Studies MeSH
- NK Cell Lectin-Like Receptor Subfamily K metabolism MeSH
- Middle Aged MeSH
- Humans MeSH
- Ligands MeSH
- Adolescent MeSH
- Cell Line, Tumor MeSH
- HSP70 Heat-Shock Proteins metabolism MeSH
- Flow Cytometry methods MeSH
- Gene Expression Regulation, Leukemic * MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- KLRK1 protein, human MeSH Browser
- NK Cell Lectin-Like Receptor Subfamily K MeSH
- Ligands MeSH
- HSP70 Heat-Shock Proteins MeSH
UNLABELLED: Membrane-bound heat shock protein 70 (HSP70) was found to be tumor-specific and was proposed as a target for immunotherapy. In the present study, we analyzed cell surface and relative gene expression of HSP70 in cell lines established from patients with different acute myeloid leukemia (AML) subtypes, together with the expression of natural killer (NK) cell activation/inhibitory ligands. MATERIALS AND METHODS: Six AML cell lines were included in this study. The relative gene expression of HSP70 was analyzed using the real-time reverse-transcriptase polymerase chain reaction. Surface expression of HSP70 and NK cell ligands was analyzed using flow cytometry. RESULTS: All cell lines overexpressed HSP70; however, its mRNA levels were not elevated. The expression of NKG2D activation ligands was heterogeneous. CONCLUSION: Our study is the first to describe long-term stationary cell surface expression of HSP70 in different subtypes of AML. Combined with the results of the gene expression experiments these data provide more evidence to the idea of a self-limiting mechanism for HSP70 expression.
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Heat-shock protein expression in leukemia
