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• W2565960060 abstract "AACR Annual Meeting-- Apr 14-18, 2007; Los Angeles, CA4267 Human T-cell leukemia virus type-I (HTLV-I) is the etiologic agent for adult T-cell leukemia (ATL) which shows various chromosomal aberrations, including aneuploidy and chromosomal instability. These abnormalities may be due to dysregulation of mitotic checkpoint proteins. Checkpoint with fork head-associated and ring finger (Chfr) is an early mitotic checkpoint gene that delays transition to metaphase in response to mitotic stress. Chfr protein, which has E3 ubiquitine ligase activity, interacts with mitotic kinase Aurora A and degrades Aurora A by ubiquitine-proteasome system. Overexpression of Aurora A transforms NIH3T3 fibroblasts and induces aneuploidy. Here we found that expression of Chfr is lost in HTLV-I-infected T-cell lines which express HTLV-I transforming protein Tax. Suppression of Chfr expression was associated with overexpression of Aurora A in these cells. Decreased expression of Chfr and overexpresion of Aurora A were also observed in primary ATL cells comparing to peripheral blood mononuclear cells (PBMCs) from healthy donors. Inducing Tax expression in JPX-9 cells, which are expressing Tax under control of the metallothionein promoter, did not affect the expression levels of Chfr and Aurora A. The 5’ CpG island of Chfr was aberrantly methylated and the methyltransferase inhibitor 5-aza-dC restored expression of Chfr in HTLV-I-infected T-cell lines, indicating that abnormal methylation in the promoter of Chfr gene inhibited the expression of this gene. Moreover, introduction of Chfr expression plasmid into HUT-102, an HTLV-I-infected T-cell line which does not express Chfr, reduced the cell growth, suggesting that loss of Chfr expression in HTLV-I-infected T-cell lines enhanced growth of the cells. To elucidate the role of overexpressed Aurora A in HTLV-I-infected T-cell lines, cells were treated with Aurora kinase inhibitor. Aurora kinase inhibitor reduced the cell viability of primary ATL cells, but did not affect that of PBMCs from healthy donors. Although the Tax-negative T-cell lines treated with Aurora kinase inhibitor underwent suppression of cell division, Aurora kinase inhibitor induced apoptosis without suppression of cell division in Tax-positive HTLV-I-infected T-cell lines. Moreover, induction of Tax protein in JPX-9 cells reduced the cell number without suppression of cell division by treatment with Aurora kinase inhibitor. These results suggest that Tax may affect cell fate after treatment of Aurora kinase inhibitor. Our findings in this study suggested that loss of Chfr and overexpression of Aurora A might contribute malignant growth and anti-apoptosis of HTLV-I-infected T-cells and these molecules are good therapeutic targets of ATL." @default.
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• W2565960060 date "2007-05-01" @default.
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• W2565960060 title "Dysregulation of mitotic checkpoint proteins Chfr and Aurora A in HTLV-I-infected T-cells" @default.
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