Fiorillo Marco, Sotgia Federica, Lisanti Michael P
Biomedical Research Centre (BRC), Translational Medicine, School of Environment and Life Sciences, University of Salford, Manchester, United Kingdom.
The Department of Pharmacy, Health and Nutritional Sciences, The University of Calabria, Cosenza, Italy.
Front Oncol. 2019 Feb 5;8:677. doi: 10.3389/fonc.2018.00677. eCollection 2018.
Here, we provide the necessary evidence that mitochondrial metabolism drives the anchorage-independent proliferation of CSCs. Two human breast cancer cell lines, MCF7 [ER(+)] and MDA-MB-468 (triple-negative), were used as model systems. To directly address the issue of metabolic heterogeneity in cancer, we purified a new distinct sub-population of CSCs, based solely on their energetic profile. We propose the term "energetic" cancer stem cells (e-CSCs), to better describe this novel cellular phenotype. In a single step, we first isolated an auto-fluorescent cell sub-population, based on their high flavin-content, using flow-cytometry. Then, these cells were further subjected to a detailed phenotypic characterization. More specifically, e-CSCs were more glycolytic, with higher mitochondrial mass and showed significantly elevated oxidative metabolism. e-CSCs also demonstrated an increased capacity to undergo cell cycle progression, as well as enhanced anchorage-independent growth and ALDH-positivity. Most importantly, these e-CSCs could be effectively targeted by treatments with either (i) OXPHOS inhibitors (DPI) or (ii) a CDK4/6 inhibitor (Ribociclib). Finally, we were able to distinguish two distinct phenotypic sub-types of e-CSCs, depending on whether they were grown as 2D-monolayers or as 3D-spheroids. Remarkably, under 3D anchorage-independent growth conditions, e-CSCs were strictly dependent on oxidative mitochondrial metabolism. Unbiased proteomics analysis demonstrated the up-regulation of gene products specifically related to the anti-oxidant response, mitochondrial energy production, and mitochondrial biogenesis. Therefore, mitochondrial inhibitors should be further developed as promising anti-cancer agents, to directly target and eliminate the "fittest" e-CSCs. Our results have important implications for using e-CSCs, especially those derived from 3D-spheroids, (i) in tumor tissue bio-banking and (ii) as a new cellular platform for drug development.
在此,我们提供了必要的证据,证明线粒体代谢驱动癌症干细胞的非锚定依赖性增殖。两种人乳腺癌细胞系,MCF7 [雌激素受体阳性(ER(+))] 和MDA-MB-468(三阴性),被用作模型系统。为了直接解决癌症中代谢异质性的问题,我们仅基于其能量特征纯化出一个新的独特癌症干细胞亚群。我们提出 “能量型” 癌症干细胞(e-CSCs)这一术语,以更好地描述这种新的细胞表型。在一个步骤中,我们首先基于其高黄素含量,使用流式细胞术分离出一个自发荧光细胞亚群。然后,对这些细胞进行进一步的详细表型特征分析。更具体地说,e-CSCs的糖酵解能力更强,线粒体质量更高,并且氧化代谢显著升高。e-CSCs还表现出细胞周期进程能力增强,以及非锚定依赖性生长和醛脱氢酶(ALDH)阳性增强。最重要的是,这些e-CSCs可以通过以下两种处理有效地靶向:(i)氧化磷酸化(OXPHOS)抑制剂(二苯基碘鎓,DPI)或(ii)细胞周期蛋白依赖性激酶4/6(CDK4/6)抑制剂(瑞博西尼)。最后,根据e-CSCs是生长为二维单层还是三维球体,我们能够区分出两种不同的表型亚型。值得注意的是,在三维非锚定依赖性生长条件下,e-CSCs严格依赖于线粒体氧化代谢。非偏向性蛋白质组学分析表明,与抗氧化反应、线粒体能量产生和线粒体生物发生特异性相关的基因产物上调。因此,线粒体抑制剂应进一步开发成为有前景的抗癌药物,以直接靶向并消除 “适应性最强” 的e-CSCs。我们的结果对于在(i)肿瘤组织生物样本库中使用e-CSCs,尤其是那些源自三维球体的e-CSCs,以及(ii)作为药物开发的新细胞平台具有重要意义。