The control of phospholipid methylation by phorbol diesters in differentiating human myeloid HL-60 leukemia cells.
The control of phospholipid methylation by phorbol diesters in differentiating human myeloid HL-60 leukemia cells.
复制标题
佛波二酯在分化人骨髓 HL-60 白血病细胞中对磷脂甲基化的控制。
DOI：
10.1093/carcin/3.8.875
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发表时间：
1982
期刊：
影响因子：
4.7
通讯作者：
Huberman,E
中科院分区：
文献类型：
--
作者：
Hoffman,DR;Huberman,E
用肿瘤启动子和分化诱导剂phorpol -12-肉豆蔻酸-13-乙酸酯（PMA）处理人HL-60早幼粒细胞白血病细胞，可刺激L-[甲基- 3h]蛋氨酸的标签进入细胞磷脂。在HL-60细胞变体中，没有观察到这种磷脂甲基化的刺激，这种细胞变体对磷酯诱导的分化具有抗性。处理后6 h检测到磷脂甲基化增强，在24-48 h达到最大水平，约为对照水平的两倍。磷脂甲基化程度与磷脂酯剂量有关。通过测定细胞裂解物中磷脂酰乙醇胺甲基转移酶的活性，证实了PMA对磷脂甲基化的刺激作用。暴露24或48小时后，HL-60细胞裂解物中的酶活性升高，但抗性细胞中的酶活性没有升高。用phorbol- 12,13 -dibutyrate或teleocidin（非phorbol-酯化合物）处理HL-60细胞后，也刺激了磷脂甲基化。这两种化学物质和PMA是HL-60细胞的肿瘤促进剂和细胞分化诱导剂。phorpol - 12,13 -diacetate和4-O-methyl PMA在HL-60细胞中不是肿瘤启动子或细胞分化诱诱剂，它们不会刺激磷脂甲基化。讨论了这些化学物质增强磷脂甲基化在HL-60细胞分化中的可能作用。
Treatment of human HL-60 promyelocytic leukemia cells with phorbol-12-myristate-13-acetate (PMA), a tumor promoter and inducer of differentiation, stimulated the incorporation of label from L-[methyl-3H]methionine into the cellular phospholipids. Such a stimulation of phospholipid methylation was not observed in an HL-60 cell variant that is resistant to phorbol ester-induced differentiation. Enhanced methylation of phospholipids was detected 6 h after treatment and reached a maximum level of about twice the control level at 24–48 h. The degree of phospholipid methylation was dependent on the phorbol ester dose. The stimulation in phospholipid methylation by PMA was confirmed by measuring the activity of phosphatidylethanolamine methyltransferase in cellular lysates. After 24 or 48 h of exposure, the enzyme activity was elevated in the HL-60 cell lysates but not in the resistant cells. Phospholipid methylation was also stimulated after treatment of the HL-60 cells with the phorbol diester phorbol-12, 13-dibutyrate or teleocidin, which is not a phorbol ester compound. These two chemicals and PMA are tumor promoters and inducers of cell differentiation in the HL-60 cells. Phorbol-12, 13-diacetate and 4-O-methyl PMA, which are not tumor promoters or inducers of cell differentiation in the HL-60 cells, did not stimulate phospholipid methylation. The possible role of enhanced phospholipid methylation in cell differentiation of the HL-60 by these chemicals is discussed.