Tanaka I, Ishihara H
Bioregulation Research Group, National Institute of Radiological Sciences, Anagawa 4-9-1, Inage-ku, Chiba, 263-8555, Japan.
Virology. 2001 Feb 1;280(1):107-14. doi: 10.1006/viro.2000.0732.
Cells of acute myeloid leukemia (AML) from C3H/He mice express an increased amount of RNA for an endogenous retrovirus-like retrotransposon, intracisternal A-particle element. We analyzed the transcription of other mouse retrotransposons in C3H-derived tumor cells and found that all the AML lines from different mice overexpress early-transposon (ETn) RNA. In contrast, only faint levels of ETn were detected in the cells from other tumors, including hepatoma and lymphoma. The polyadenylation sites of the ETn RNA in the AML cells varied. We also determined the binding site for the nuclear extract of the AML cells in the long terminal repeat sequence of ETn. The overexpression of ETn as a common phenotype of AML cells suggests that myeloid cells with this phenotype are the origin of all the AML cells or that the phenotype is acquired during leukemogenesis.
来自C3H/He小鼠的急性髓系白血病(AML)细胞中,一种内源性逆转录病毒样逆转座子——脑池内A颗粒元件的RNA表达量增加。我们分析了C3H来源的肿瘤细胞中其他小鼠逆转座子的转录情况,发现来自不同小鼠的所有AML细胞系均过度表达早期转座子(ETn)RNA。相比之下,在包括肝癌和淋巴瘤在内的其他肿瘤细胞中,仅检测到微弱水平的ETn。AML细胞中ETn RNA的聚腺苷酸化位点各不相同。我们还确定了AML细胞核提取物在ETn长末端重复序列中的结合位点。ETn的过度表达作为AML细胞的一种常见表型,表明具有这种表型的髓系细胞是所有AML细胞的起源,或者该表型是在白血病发生过程中获得的。