Tumour necrosis factor and interferon are selectively cytostatic in vitro for hormone-dependent and hormone-independent human breast cancer cells

Tumour necrosis factor and interferon are selectively cytostatic in vitro for hormone-dependent and hormone-independent human breast cancer cells
复制标题

DOI:
10.1016/s0959-8049(96)00273-0
复制
发表时间:
1996-12-01
影响因子:
8.4
通讯作者:
Eppenberger, U
Eppenberger, U
中科院分区:
医学1区
文献类型:
--
作者:
Mueller, H;Flury, N;Eppenberger, U

文献摘要

被引文献

相似文献

由于实验研究表明,肿瘤坏死因子-α(TNF-α)具有强效的抗肿瘤活性,可以与细胞因子增强,我们测试了TNF-α与干扰素-γ(IFN-γ)对不同的人乳腺癌细胞系的疗效,特别是比较依赖和非依赖表型。TNF-α可抑制乳腺癌细胞MCF-7、ZR-75-1和T47-D的生长,半数最大浓度为0.25 nM。相比之下,单独TNF-α不影响非肿瘤依赖性细胞MDA-MB-231和HS 578 T的生长,但是当一起使用IFN-γ和TNF-α时观察到协同抑制。原癌基因C-MYC的mRNA作为细胞活化的细胞内指标,在TNF-α存在下在MCF-7细胞中显著增加。在MDA-MB-231细胞中,这种mRNA仅在TNF-α和IFN-γ存在下增加,而表面TNF受体的数量没有变化。这些发现表明,TNF-α联合IFN-γ治疗可能提供一种成功的方法来克服晚期乳腺肿瘤的细胞异质性。版权所有(C)1996 Elsevier Science Ltd
Since experimental studies have shown that tumour necrosis factor-alpha (TNF-alpha) has potent antitumour activity that can be potentiated with cytokines, we tested the efficacy of TNF-alpha with interferon-gamma (IFN-gamma) on different human breast cancer cell lines, particularly comparing hormone-dependent and -independent phenotypes. TNF-alpha inhibited the growth of hormone-dependent human MCF-7, ZR-75-1 and T47-D breast cancer cells with a half maximal concentration of 0.25 nM. In contrast, the growth of hormone-independent cells MDA-MB-231 and HS578T was not affected by TNF-alpha alone, but a synergistic inhibition was observed when using IFN-gamma and TNF-alpha together. The mRNA for the proto-oncogene C-MYC, as an intracellular indicator of cell activation, was significantly increased in MCF-7 cells in the presence of TNF-alpha. In MDA-MB-231 cells this mRNA was increased only in the presence of both TNF-alpha and IFN-gamma, without a change in the number of surface TNF receptors. These findings indicate that TNF-alpha treatment in combination with IFN-gamma may provide a successful approach to overcome the cellular heterogeneity of advanced breast tumours. Copyright (C) 1996 Elsevier Science Ltd