Depraetere S, Joniau M
Interdisciplinary Research Center, Laboratory of Biochemistry, Kortrijk, Belgium.
Leuk Res. 1995 Nov;19(11):803-9. doi: 10.1016/0145-2126(95)00060-7.
After prolonged incubation times of 72 h IFN alpha 2a and IFN beta 1 significantly reduced cell growth in the myelomonocytic U937 and THP1 cell lines. IFN gamma showed only slight growth inhibitory activities. IFN activities were potentiated by the highly polar differentiation inducer dimethylsulphoxide, which is similar to our previous study on tumor necrosis factor (TNF). However, in contrast with TNF, none of the interferon types induced cell cytotoxicity or DNA fragmentation. Like DMSO, all interferons potentiated TNF-induced cytotoxicity, IFN beta 1 and IFN gamma being the most potent in this respect. When applied together, DMSO and IFN gamma enhanced TNF-mediated cell lysis in either an additive (in the case of U937, THP1, HL60 cells) or a synergistic (in the case of KG1) manner, suggesting that the mechanisms of the potentiating activity of DMSO and IFN gamma are different. The potential role of the simultaneous use of DMSO-related molecules, and TNF and/or IFN in leukemic cancer chemotherapy is discussed.
在长达72小时的孵育时间后，干扰素α2a和干扰素β1显著降低了髓单核细胞系U937和THP1细胞的生长。干扰素γ仅表现出轻微的生长抑制活性。高极性分化诱导剂二甲基亚砜增强了干扰素的活性，这与我们之前关于肿瘤坏死因子（TNF）的研究相似。然而，与TNF不同的是，任何一种干扰素类型均未诱导细胞毒性或DNA片段化。与二甲基亚砜一样，所有干扰素均增强了TNF诱导的细胞毒性，其中干扰素β1和干扰素γ在这方面最为有效。当联合使用时，二甲基亚砜和干扰素γ以相加的方式（在U937、THP1、HL60细胞的情况下）或协同的方式（在KG1细胞的情况下）增强了TNF介导的细胞裂解，这表明二甲基亚砜和干扰素γ增强活性的机制不同。本文讨论了同时使用与二甲基亚砜相关的分子以及TNF和/或干扰素在白血病癌症化疗中的潜在作用。
