Ectopic cyclin D1 expression blocks STI571-induced erythroid differentiation of K562 cells
Autor: | Satsuki Iwase, Yusuke Furukawa, Hisashi Yamada, Shinobu Saito, Takeshi Kawano, Yasuhiko Kano, Junko Horiguchi-Yamada |
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Rok vydání: | 2004 |
Předmět: |
Cancer Research
Lactams Macrocyclic Cyclin D Down-Regulation chemical and pharmacologic phenomena Transfection Piperazines Cyclin D1 Cyclin-dependent kinase hemic and lymphatic diseases Benzoquinones Humans Glycophorin Glycophorins Enzyme Inhibitors Phosphorylation Erythroid Precursor Cells Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase Kinases Mitogen-Activated Protein Kinase 3 biology Chemistry Quinones Cell Differentiation Hematology Protein-Tyrosine Kinases Molecular biology Cell biology Pyrimidines Rifabutin Oncology Drug Resistance Neoplasm Mitogen-activated protein kinase Benzamides Imatinib Mesylate biology.protein Ectopic expression Mitogen-Activated Protein Kinases K562 Cells Cyclin A2 Signal Transduction K562 cells |
Zdroj: | Leukemia Research. 28:623-629 |
ISSN: | 0145-2126 |
DOI: | 10.1016/j.leukres.2003.10.022 |
Popis: | Bcr-Abl tyrosine kinase inhibitor induces apoptosis and erythroid differentiation of K562 cells. During this erythroid differentiation, c-Myc and cyclin D1 transcripts are transiently downregulated. Accordingly, we studied the effect of cyclin D1 overexpression on erythroid differentiation. After treatment with 250 nM STI571, 90% of K562 and 25% of K562/D1 cells underwent erythroid differentiation. The basal expression of glycophorin A in K562/D1 cells was markedly diminished compared with that by parental cells. STI571 treatment failed to induce glycophorin A expression in K562/D1 cells. During STI571 treatment, ERK activity was downregulated in parental cells, while it was constantly activated in K562/D1 cells. These results suggest that ectopic expression of cyclin D1 causes the resistance of K562 cells to erythroid differentiation by modulating ERK regulation. |
Databáze: | OpenAIRE |
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