Cisplatin-induced apoptosis in HL-60 human promyelocytic leukemia cells: differential expression of BCL2 and novel apoptosis-related gene BCL2L12
Autor: | Nikos Katsaros, Kostas V. Floros, Hellinida Thomadaki, George Lallas, Maroulio Talieri, Andreas Scorilas |
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Rok vydání: | 2004 |
Předmět: |
DNA
Complementary Transcription Genetic Cell Survival Muscle Proteins Apoptosis HL-60 Cells DNA laddering Biology General Biochemistry Genetics and Molecular Biology History and Philosophy of Science Downregulation and upregulation hemic and lymphatic diseases medicine Humans RNA Messenger Gene DNA Primers Cisplatin Regulation of gene expression Base Sequence General Neuroscience Molecular biology Genes bcl-2 Gene Expression Regulation Neoplastic Kinetics Proto-Oncogene Proteins c-bcl-2 Cell culture DNA fragmentation medicine.drug |
Zdroj: | Annals of the New York Academy of Sciences. 1010 |
ISSN: | 0077-8923 |
Popis: | The anti-apoptotic molecule BCL2 delays cell-cycle entry from quiescence. We have recently cloned a new member of the BCL2 family of apoptosis-related genes, BCL2L12. In the present study, the expression of BCL2 and BCL2L12 genes during cisplatin-induced apoptosis in HL-60 leukemic cells was investigated. The kinetics of apoptosis induction and cell toxicity were evaluated by DNA laddering and the MTT method, respectively. BCL2 and BCL2L12 expression was analyzed by RT-PCR using gene-specific primers. The ratio of apoptotic cells increased with increasing concentrations of cisplatin and exposure time of cell culture to the drug. Gradual, time-dependent downregulation of BCL2 gene was observed during cisplatin treatment. Up-regulation of BCL2L12 was observed 3 h (no DNA fragmentation) and 6 h (initiation of the DNA fragmentation) after treatment with cisplatin, followed by a decrease of its expression after 12-h continuous treatment with the drug. It is known that the main anti-carcinogenic effect of cisplatin is due to the induction of cell apoptosis. Present results indicate that downregulation of the BCL2 and upregulation of the BCL2L12 gene may be the underlying mechanisms. |
Databáze: | OpenAIRE |
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