5-Aminolevulinate Synthase Expression and Hemoglobin Synthesis in a Human Myelogenous Leukemia Cell Line

We examined the effect of hemin, TGF-β1 and cytosine arabinoside (Ara-C) on the levels of mRNAs for the erythroid-specific 5-aminolevulinate synthase (ALAS-E) and γ-globin in various human myelogenous leukemia cell lines. Detailed analyses were also made using one of them, YN-1, which was isolated a...

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Bibliographic Details
Published in:Journal of biochemistry (Tokyo) 1997-03, Vol.121 (3), p.487-495
Main Authors: Nagai, Tadashi, Harigae, Hideo, Furuyama, Kazumichi, Munakata, Hiroshi, Hayashi, Norio, Endo, Kazuyasu, Sassa, Shigeru, Yamamoto, Masayuki
Format: Article
Language:English
Subjects:
5-aminolevulinate synthase
5-Aminolevulinate Synthetase - genetics
Cell Line
Cytarabine - pharmacology
Fibroblast Growth Factors - pharmacology
Gene Expression Regulation, Enzymologic - drug effects
Gene Expression Regulation, Neoplastic - drug effects
globin mRNA
hemin
Hemin - pharmacology
hemoglobin synthesis
Hemoglobins - biosynthesis
Hemoglobins - genetics
human leukemia cells
Humans
Leukemia, Myeloid - enzymology
Leukemia, Myeloid - metabolism
Leukemia, Myeloid - pathology
RNA, Messenger - genetics
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Summary:We examined the effect of hemin, TGF-β1 and cytosine arabinoside (Ara-C) on the levels of mRNAs for the erythroid-specific 5-aminolevulinate synthase (ALAS-E) and γ-globin in various human myelogenous leukemia cell lines. Detailed analyses were also made using one of them, YN-1, which was isolated and established in culture from a patient with chronic myelogenous leukemia. Our results demonstrate that γ-globin protein level and the percentage of benzidine-positive cells in the cell line increased markedly (10- to 30-fold) upon treatment with hemin, TGF-β1, or Ara-C. In contrast, γglobin mRNA was already markedly expressed prior to treatment in 4 out of 9 cell lines examined, including YN-1, and the level increased only marginally after treatment with hemin. ALAS-E mRNA levels were increased in YN-1 cells after treatment with TGF-β1 and Ara-C, while hemin treatment had little effect. These results indicate that heme supply is insufficient in YN-1 cells and suggest that hemin increases hemoglobin synthesis principally at the post-transcriptional level, whereas TGF-β1 and Ara-C stimulate hemoglobin synthesis by activating efficient endogenous heme supply in the cells.
ISSN:0021-924X
DOI:10.1093/oxfordjournals.jbchem.a021613