1988 Fiscal Year Final Research Report Summary
Studies on biochemical mechanisms in the commitment of leukemic cell differentiation into various cell lineages
| Project/Area Number |
62570544
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | Kyoto University |
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Principal Investigator |
SAWADA Hiroyoshi The Faculty of Medicine, Kyoto University, 医学部, 講師 (30093248)
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| Project Period (FY) |
1987 – 1988
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| Keywords | HL-60 cell / K-562 cell / Differentiation / dbcAMP / Staurosporine / Lysozyme mRNA / 蛋白合成 |
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| Research Abstract |
The role of second messengers on differentiation of HL-60 cells and K-562 cells was investigated. HL-60 cell differentiation induced by various compounds except TPA was enhanced by dbcAMP, an activator of protein kinase A, and staurosporine, an inhibitor of protein kinase C. On the other hand OAG, an activator of protein kinase C, enhanced K-562 cell differentiation into erythrocyte lineage induced by hemin. However OAG did not enhance K-562 cell differentiation induced by other agents such as Ara-C, and actinomycin-D.
Expression of lysozyme mRNA was investigated in the process of HL-60 cell differentiation. Northern blot analysis revealed that lysozyme mRNA was expressed as cell differentiation progressed, and this expression was completely inhibited by cycloheximide, suggesting new protein synthesis is essential before differentiation related phenotypes are expressed.
Present results indicate that both activation of second messengers and new protein synthesis are necessary for the signal transduction from a commitment step to a phenotype expression step in leukemic cell differentiation.
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