Expression levels of ASNS in mesenchymal stromal cells in childhood acute lymphoblastic leukemia
| Autor: | Christianna Choulaki, Chryssoula Perdikogianni, Maria Kalmanti, Eftichia Stiakaki, Helen Dimitriou |
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| Rok vydání: | 2013 |
| Předmět: |
medicine.medical_specialty
Asparaginase Asparagine synthetase Gene Expression Biology Gene Expression Regulation Enzymologic chemistry.chemical_compound Internal medicine Gene expression medicine Humans RNA Messenger Stem Cell Niche Child Cells Cultured Regulation of gene expression Hematology Mesenchymal stem cell Aspartate-Ammonia Ligase Mesenchymal Stem Cells Precursor Cell Lymphoblastic Leukemia-Lymphoma Molecular biology Up-Regulation Haematopoiesis medicine.anatomical_structure chemistry Bone marrow |
| Zdroj: | International journal of hematology. 99(3) |
| ISSN: | 1865-3774 |
| Popis: | Increased levels of asparagine synthetase (ASNS), an enzyme producing intracellular asparagine, have been implicated in the development of asparaginase resistance. The aim of this study was to assess ASNS mRNA and protein expression in bone marrow cell populations of children with acute lymphoblastic leukemia (ALL). Bone marrow mononuclear cells at diagnosis, day 33 of treatment, and after completion of chemotherapy were isolated and studied. ASNS mRNA expression was assessed by real-time PCR, and protein levels by Western blot. Our results indicate that MSC ASNS mRNA expression is upregulated in ALL samples compared to controls. ASNS expression of mesenchymal stromal cells (MSC) was found to be 2.3 times higher than that of blasts at diagnosis of ALL. We also observed that the values of the ASNS mRNA of MSC seem to reach a peak at diagnosis, and tend to decline with treatment. No correlation was found between the ASNS mRNA and protein levels. Chemotherapy does not exert any effect on the protein expression. Variability of asparaginase-induced effect may be attributable to factors involved in the interaction of hematopoietic cells with their microenvironment. |
| Databáze: | OpenAIRE |
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