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UBE2Q1, as a Down Regulated Gene in Pediatric Acute Lymphoblastic Leukemia
Ubiquitin - proteasome system (UPS), the major protein degradation pathway in the cells, typically degrades short - lived and damaged proteins and regulates growth and stress responses. This pathway is altered in various cancers, including Acute Lymphoblastic Leukemia (ALL). ALL begins with a change...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Babol University of Medical Sciences
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4082811/ https://www.ncbi.nlm.nih.gov/pubmed/25035859 |
Sumario: | Ubiquitin - proteasome system (UPS), the major protein degradation pathway in the cells, typically degrades short - lived and damaged proteins and regulates growth and stress responses. This pathway is altered in various cancers, including Acute Lymphoblastic Leukemia (ALL). ALL begins with a change in bone marrow cells and is the most common type of leukemia in children under 15 years. UBE2Q1 as a new characterized gene of E2 enzyme family is located on chromosome 1 and reported to be altered in some malignancies. In this study, we aimed to explore the expression pattern of UBE2Q1 gene in children with ALL. For this purpose, a series of RT - PCR and quantitative RT - PCR were performed on a collection of 20 bone marrow samples of ALL patients and the same number of whole blood samples of age - matched normal subjects. Gel electrophoresis of RT - PCR products revealed the expression of UBE2Q1 mRNA in most of the normal (90%) and about half of the leukemic (45%) samples. QRT - PCR data indicated that only 1 patient out of 20 (5%) showed up regulation of the gene (> 2 folds). In 4 patients (20%), the expression of UBE2Q1 mRNA was equivocal (from 1/2 to 2) and in 15 cases (75%), the gene was down regulated (> 1/2) when compared to the normal samples. In conclusion, down regulation of UBE2Q1 in the majority of the leukemic samples suggests its potential implication in the pathogenesis of ALL. UBE2Q1 can be considered as a molecular marker and a candidate targeting to treat ALL in the future. |
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