Ozsvari Bela, Sotgia Federica, Lisanti Michael P
Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC), University of Salford, Greater Manchester, United Kingdom.
The Paterson Institute, University of Manchester, Withington, United Kingdom.
Aging (Albany NY). 2018 Feb 19;10(2):229-240. doi: 10.18632/aging.101384.
Tri-phenyl-phosphonium (TPP) is a non-toxic chemical moiety that functionally behaves as a mitochondrial targeting signal (MTS) in living cells. Here, we explored the hypothesis that TPP-related compounds could be utilized to inhibit mitochondria in cancer stem cells (CSCs). We randomly selected 9 TPP-related compounds for screening, using an ATP depletion assay. Based on this approach, five compounds were identified as "positive hits"; two had no detectable effect on ATP production. Remarkably, this represents a >50% hit rate. We validated that the five positive hit compounds all inhibited oxygen consumption rates (OCR), using the Seahorse XFe96 metabolic flux analyzer. Interestingly, these TPP-related compounds were non-toxic and had little or no effect on ATP production in normal human fibroblasts, but selectively targeted adherent "bulk" cancer cells. Finally, these positive hit compounds also inhibited the propagation of CSCs in suspension, as measured functionally using the 3D mammosphere assay. Therefore, these TPP-related compounds successfully inhibited anchorage-independent growth, which is normally associated with a metastatic phenotype. Interestingly, the most effective molecule that we identified contained two TPP moieties (i.e., bis-TPP). More specifically, 2-butene-1,4-bis-TPP potently and selectively inhibited CSC propagation, with an IC-50 < 500 nM. Thus, we conclude that the use of bis-TPP, a "dimeric" mitochondrial targeting signal, may be a promising new approach for the chemical eradication of CSCs. Future studies on the efficacy of 2-butene-1,4-bis-TPP and its derivatives are warranted. In summary, we show that TPP-related compounds provide a novel chemical strategy for effectively killing both i) "bulk" cancer cells and ii) CSCs, while specifically minimizing or avoiding off-target side-effects in normal cells. These results provide the necessary evidence that "normal" mitochondria and "malignant" mitochondria are truly biochemically distinct, removing a significant barrier to therapeutically targeting cancer metabolism.
三苯基膦(TPP)是一种无毒的化学基团,在活细胞中其功能表现为线粒体靶向信号(MTS)。在此,我们探讨了一种假说,即与TPP相关的化合物可用于抑制癌症干细胞(CSC)中的线粒体。我们随机选择了9种与TPP相关的化合物,采用ATP消耗测定法进行筛选。基于这种方法,鉴定出5种化合物为“阳性命中物”;两种对ATP生成没有可检测到的影响。值得注意的是,这代表了超过50%的命中率。我们使用海马XFe96代谢通量分析仪验证了这5种阳性命中化合物均能抑制氧消耗率(OCR)。有趣的是,这些与TPP相关的化合物无毒,对正常人成纤维细胞中的ATP生成几乎没有影响,但能选择性地靶向贴壁的“大量”癌细胞。最后,这些阳性命中化合物还抑制了悬浮培养的CSC的增殖,通过使用3D乳腺球测定法进行功能测定。因此,这些与TPP相关的化合物成功抑制了不依赖贴壁的生长,而这通常与转移表型相关。有趣的是,我们鉴定出的最有效的分子含有两个TPP基团(即双TPP)。更具体地说,2-丁烯-1,4-双TPP能有效且选择性地抑制CSC增殖,IC-50 < 500 nM。因此,我们得出结论,使用双TPP这种“二聚体”线粒体靶向信号,可能是化学根除CSC的一种有前景的新方法。有必要对2-丁烯-1,4-双TPP及其衍生物的疗效进行进一步研究。总之,我们表明与TPP相关的化合物提供了一种新的化学策略,既能有效杀死i)“大量”癌细胞,又能杀死ii)CSC,同时特别地将正常细胞中的脱靶副作用降至最低或避免。这些结果提供了必要的证据,证明“正常”线粒体和“恶性”线粒体在生物化学上确实不同,消除了治疗性靶向癌症代谢的一个重大障碍。