Wt-p53 action in human leukaemia cell lines corresponding to different stages of differentiation
Autor: | Giovanni Blandino, Ada Sacchi, Mg Rizzo, S Giuliacci, Raffaella Scardigli, Marco Crescenzi, Silvia Soddu, Sergio Ferrari, Barbara Cristofanelli, A Zepparoni |
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Rok vydání: | 1998 |
Předmět: |
p53
Cancer Research Tumor suppressor gene Cell Survival Cellular differentiation leukaemia differentiation apoptosis gene therapy Cell Apoptosis Cell Count HL-60 Cells DNA Fragmentation Biology hemic and lymphatic diseases Precursor cell Gene expression medicine Humans Leukemia Genetic transfer Cell Differentiation Genetic Therapy Transfection Genes p53 medicine.anatomical_structure Oncology Immunology Cancer research Research Article K562 cells |
Zdroj: | British Journal of Cancer ResearcherID |
ISSN: | 1532-1827 0007-0920 |
DOI: | 10.1038/bjc.1998.236 |
Popis: | Recent studies support the potential application of the wt-p53 gene in cancer therapy. Expression of exogenous wt-p53 suppresses a variety of leukaemia phenotypes by acting on cell survival, proliferation and/or differentiation. As for tumour gene therapy, the final fate of the neoplastic cells is one of the most relevant points. We examined the effects of exogenous wt-p53 gene expression in several leukaemia cell lines to identify p53-responsive leukaemia. The temperature-sensitive p53Val135 mutant or the human wt-p53 cDNA was transduced in leukaemia cell lines representative of different acute leukaemia FAB subtypes, including M1 (KG1), M2 (HL-60), M3 (NB4), M5 (U937) and M6 (HEL 92.1.7), as well as blast crisis of chronic myelogenous leukaemia (BC-CML: K562, BV173) showing diverse differentiation features. By morphological, molecular and biochemical analyses, we have shown that exogenous wt-p53 gene expression induces apoptosis only in cells corresponding to M1, M2 and M3 of the FAB classification and in BC-CML showing morphological and cytochemical features of undifferentiated blast cells. In contrast, it promotes differentiation in the others. Interestingly, cell responsiveness was independent of the vector used and the status of the endogenous p53 gene. Images Figure 1 Figure 2 Figure 6 Figure 7 |
Databáze: | OpenAIRE |
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