Steinmetz Julia, Senkowski Wojciech, Lengqvist Johan, Rubin Jenny, Ossipova Elena, Herman Stephanie, Larsson Rolf, Jakobsson Per-Johan, Fryknäs Mårten, Kultima Kim
Division of Rheumatology, Department of Medicine, Solna, Karolinska Institutet and Karolinska University Hospital, SE-171 76 Stockholm, Sweden.
Department of Medical Sciences, Cancer Pharmacology and Computational Medicine, Uppsala University, Uppsala SE-751 05, Sweden.
ACS Omega. 2020 Jul 6;5(28):17242-17254. doi: 10.1021/acsomega.0c01419. eCollection 2020 Jul 21.
We have previously identified selective upregulation of the mevalonate pathway genes upon inhibition of oxidative phosphorylation (OXPHOS) in quiescent cancer cells. Using mass spectrometry-based proteomics, we here investigated whether these responses are corroborated on the protein level and whether proteomics could yield unique insights into context-dependent biology. HCT116 colon carcinoma cells were cultured as monolayer cultures, proliferative multicellular tumor spheroids (P-MCTS), or quiescent (Q-MCTS) multicellular tumor spheroids and exposed to OXPHOS inhibitors: nitazoxanide, FCCP, oligomycin, and salinomycin or the HMG-CoA-reductase inhibitor simvastatin at two different doses for 6 and 24 h. Samples were processed using an in-depth bottom-up proteomics workflow resulting in a total of 9286 identified protein groups. Gene set enrichment analysis showed profound differences between the three cell systems and confirmed differential enrichment of hypoxia, OXPHOS, and cell cycle progression-related protein responses in P-MCTS and Q-MCTS. Treatment experiments showed that the observed drug-induced alterations in gene expression of metabolically challenged cells are not translated directly to the protein level, but the results reaffirmed OXPHOS as a selective vulnerability of quiescent cancer cells. This work provides rationale for the use of deep proteome profiling to identify context-dependent treatment responses and encourages further studies investigating metabolic processes that could be co-targeted together with OXPHOS to eradicate quiescent cancer cells.
我们之前已经确定,在静止癌细胞中抑制氧化磷酸化(OXPHOS)后,甲羟戊酸途径基因会选择性上调。在此,我们使用基于质谱的蛋白质组学技术,研究这些反应在蛋白质水平上是否得到证实,以及蛋白质组学能否为背景依赖性生物学提供独特见解。将HCT116结肠癌细胞培养为单层培养物、增殖性多细胞肿瘤球体(P-MCTS)或静止性(Q-MCTS)多细胞肿瘤球体,并使其暴露于OXPHOS抑制剂:硝唑尼特、羰基氰化物4-(三氟甲氧基)苯腙(FCCP)、寡霉素和沙利霉素,或两种不同剂量的HMG-CoA还原酶抑制剂辛伐他汀,处理6小时和24小时。使用深度自下而上的蛋白质组学工作流程对样品进行处理,共鉴定出9286个蛋白质组。基因集富集分析显示,这三种细胞系统之间存在显著差异,并证实了P-MCTS和Q-MCTS中缺氧、OXPHOS和细胞周期进程相关蛋白质反应的差异富集。处理实验表明,在代谢受挑战的细胞中观察到的药物诱导的基因表达变化并未直接转化为蛋白质水平,但结果再次证实OXPHOS是静止癌细胞的选择性脆弱点。这项工作为使用深度蛋白质组分析来识别背景依赖性治疗反应提供了理论依据,并鼓励进一步研究调查可与OXPHOS共同靶向以根除静止癌细胞的代谢过程。