The growth-regulatory role of B-cell-specific activator protein in NZB malignant B-1 cells
| Autor: | Nicholas M. Ponzio, Elizabeth Raveche, Yi-Chu Lin, Zenaida Garcia, Ming Zhang, Siew Yen Chong, Frederick D. Coffman |
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| Rok vydání: | 2001 |
| Předmět: |
G2 Phase
Cancer Research Antigens CD19 Immunology B-Lymphocyte Subsets Mice Inbred Strains Biology medicine.disease_cause Mice chemistry.chemical_compound medicine Animals Humans Immunology and Allergy Mitosis B cell Gene Rearrangement Colcemid Cell growth Demecolcine PAX5 Transcription Factor Nuclear Proteins Gene rearrangement Oligonucleotides Antisense Cell cycle Leukemia Lymphocytic Chronic B-Cell Molecular biology DNA-Binding Proteins medicine.anatomical_structure Oncology chemistry Carcinogenesis Cell Division Transcription Factors |
| Zdroj: | Cancer Immunology, Immunotherapy. 50:41-50 |
| ISSN: | 1432-0851 0340-7004 |
| DOI: | 10.1007/s002620000165 |
| Popis: | The transcription factor B-cell-specific activator protein (BSAP) plays an important role in B-cell development. We explored the involvement of BSAP in the growth regulation of malignant B-1 cells derived from the NZB murine model of human chronic lymphocytic leukemia. BSAP protein was found in normal B-2 cells, elevated in normal B-1 cells, and highest in NZB malignant B-1 cells. When these malignant B-1 cells were treated with antisense oligonucleotides for BSAP, their growth was inhibited with a G2/M phase arrest. In contrast, B cell lines that did not appear to be of B-1 origin (IgG+/B220+/BSAPlow) were unaffected by treatment with antisense BSAP oligonucleotides. Centrifugal elutriation experiments showed that BSAP mRNA was expressed at the highest levels in the G2/M phases in malignant B-1 cells. Treatment with demecolcine (Colcemid), a known mitotic blocker, resulted in a decrease in the level of BSAP gene expression in malignant B-1 cells, further demonstrating links between BSAP expression and successful G2/M transition in the cell cycle. These data suggest a correlation between BSAP and the development of B-1 malignancy, perhaps through the regulation of cell-cycle progression. |
| Databáze: | OpenAIRE |
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