Genes encoded within 8q24 on the amplicon of a large extrachromosomal element are selectively repressed during the terminal differentiation of HL-60 cells
Mutation Research : Fundamental and Molecular Mechanisms of Mutagenesis 640 巻 1-2 号
97-106 頁
2008 発行
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タイトル ( eng ) |
Genes encoded within 8q24 on the amplicon of a large extrachromosomal element are selectively repressed during the terminal differentiation of HL-60 cells
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作成者 |
Ike Fumio
Murata Takehide
Obata Yuichi
Utiyama Hiroyasu
Yokoyama Kazunari K.
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収録物名 |
Mutation Research : Fundamental and Molecular Mechanisms of Mutagenesis
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巻 | 640 |
号 | 1-2 |
開始ページ | 97 |
終了ページ | 106 |
抄録 |
Human acute myeloblastic leukemia HL-60 cells become resistant to differentiation during longterm cultivation. After 150 passages, double minute chromosomes (dmins) found in early-passaged cells are replaced by large extrachromosomal elements (LEEs). In a DNA library derived from a purified fraction of LEEs, 12.6% (23/183) of clones were assigned to 8q24 and 9.2% (17/183) were assigned to 14q11 in the human genome. Fluorescence in situ hybridization (FISH) revealed a small aberrant chromosome, which had not been found in early-passaged cells, in addition to the purified LEEs. We determined that each LEE consisted of six discontinuous segments in a region that extended for 4.4 Mb over the 8q24 locus. Five genes, namely, Myc (a proto-oncogene), NSMCE2 (for a SUMO ligase), CCDC26 (for a retinoic acid-dependent modulator of myeloid differentiation), TRIB1 (for a regulator of MAPK kinase) and LOC389637 (for a protein of unknown function), were encoded by the amplicon. Breaks in the chromosomal DNA within the amplicon were found in the NSMCE2 and CCDC26 genes. The discontinuous structure of the amplicon unit of the LEEs was identical with that of dmins in HL60 early-passaged cells. The difference between them seemed, predominantly, to be the number (10 to 15 copies per LEE versus2 or 3 copies per dmin) of constituent units. Expression of the Myc, NSMCE2, CCDC26 and LOC389637 and TRIB1genes was constitutive in all lines of HL-60 cells and that of the first four genes was repressed during the terminal differentiation of earlypassaged HL-60 cells. We also detected abnormal transcripts of CCDC26. Our results suggest that these genes were selected during the development of amplicons. They might be amplified and, sometimes, truncated to contribute to the maintenance of HL-60 cells in an undifferentiated state.
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著者キーワード |
gene amplification
genetic instability
double minute chromosome
large extrachromosomal element
terminal differentiation
apoptosis
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NDC分類 |
生物科学・一般生物学 [ 460 ]
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言語 |
英語
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資源タイプ | 学術雑誌論文 |
出版者 |
Elsevier B.V.
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発行日 | 2008 |
権利情報 |
Copyright (c) 2007 Elsevier B.V.
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出版タイプ | Author’s Original(十分な品質であるとして、著者から正式な査読に提出される版) |
アクセス権 | オープンアクセス |
収録物識別子 |
[NCID] AA11032004
[ISSN] 0027-5107
[DOI] 10.1016/j.mrfmmm.2007.12.008
[DOI] http://dx.doi.org/10.1016/j.mrfmmm.2007.12.008
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