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阿昔洛韦和赫比霉素A协同抑制人髓性白血病K562细胞的增殖并诱导其红系分化。

Acycloguanosine and herbimycin A co-operatively inhibit proliferation and induce erythrodifferentiation of human myeloid leukemia K562 cells.

作者信息

Honma Y

机构信息

Department of Chemotherapy, Saitama Cancer Center Research Institute, Japan.

出版信息

Leuk Res. 1994 Nov;18(11):851-4. doi: 10.1016/0145-2126(94)90166-x.

DOI:10.1016/0145-2126(94)90166-x
PMID:7967712
Abstract

Acycloguanosine (9-[(2-hydroxyethoxy)methyl]guanosine) induced human erythroleukemia K562 cells to differentiate into hemoglobin-producing cells, and cell growth was highly sensitive to this nucleoside analog. Herbimycin A also induced erythrodifferentiation of the cells, and selectively inhibited proliferation of the cells. Selective inhibition of the proliferation in K562 cells was greatly enhanced by combined treatment with acycloguanosine and herbimycin A, while the growth of another erythroleukemia cell line without bcr/abl gene (HEL) and normal mouse bone marrow cells was hardly affected by the treatment.

摘要

阿昔洛韦(9-[(2-羟基乙氧基)甲基]鸟苷)可诱导人红白血病K562细胞分化为产生血红蛋白的细胞,且细胞生长对这种核苷类似物高度敏感。赫比霉素A也可诱导这些细胞发生红系分化,并选择性抑制细胞增殖。阿昔洛韦与赫比霉素A联合处理可大大增强对K562细胞增殖的选择性抑制,而另一种无bcr/abl基因的红白血病细胞系(HEL)和正常小鼠骨髓细胞的生长几乎不受该处理的影响。

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