Department of Pharmaceutical Sciences, Center for Pharmaceutical Biotechnology and Nanomedicine, Northeastern University, Boston, MA, USA.
Department of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, Boston, MA, USA.
Int J Pharm. 2017 Oct 30;532(1):149-156. doi: 10.1016/j.ijpharm.2017.08.095. Epub 2017 Aug 24.
Cancer cells increase their metabolism to produce the energy and biomolecules necessary for growth and proliferation. Thus, energy metabolism pathways may serve as targets for anti-cancer therapy. NCL-240 is a second generation anti-cancer drug belonging to the PITenins class of PI3K-Akt inhibitors. Our analysis suggested that NCL-240 caused disruptions in mitochondrial oxidative phosphorylation and up-regulated glycolysis, as evidenced by the loss of NMR peaks for the amino acid products derived from the TCA cycle along with presence of only lactate peaks and the loss of glucose peaks. NCL-240 was combined with 2-deoxy-d-glucose (2-DG) in early proof-of-concept studies on multiple cell lines. 2-DG enhanced cell death response to NCL-240 administration, with cytotoxicity results similar to those under hypoglycemic conditions. In further studies, NCL-240 encapsulated in phosphatidylcholine/cholesterol liposomes was combined with freely dissolved 2-DG. Cell cycle analysis of sensitive and resistant strains of A2780 cells treated with combinations of NCL-240/2-DG pointed to a G0/G1 phase arrest for 80-90% of the total, indicating an inability to grow and divide. Cytotoxicity studies with in vitro cancer cell monolayer models confirmed the results of cell cycle analysis. Significant improvements in cytotoxicity with combination treatments over control and individual treatments were seen in multiple cell lines. NCI/ADR-RES cancer cell spheroids further demonstrated the effectiveness of a NCL-240/2-DG combination.
癌细胞增加其代谢以产生生长和增殖所需的能量和生物分子。因此,能量代谢途径可以作为抗癌治疗的靶点。NCL-240 是一种属于 PI3K-Akt 抑制剂的 PITenins 类的第二代抗癌药物。我们的分析表明,NCL-240 导致线粒体氧化磷酸化中断,并上调糖酵解,这表现在 TCA 循环衍生的氨基酸产物的 NMR 峰消失,而只有乳酸峰存在,以及葡萄糖峰的消失。在对多种细胞系的早期概念验证研究中,NCL-240 与 2-脱氧-d-葡萄糖(2-DG)联合使用。2-DG 增强了对 NCL-240 给药的细胞死亡反应,细胞毒性结果与低血糖条件下相似。在进一步的研究中,用磷脂酰胆碱/胆固醇脂质体包封的 NCL-240 与游离溶解的 2-DG 结合。用 NCL-240/2-DG 组合处理的敏感和耐药 A2780 细胞株的细胞周期分析表明,总细胞的 80-90%处于 G0/G1 期停滞,表明无法生长和分裂。体外癌细胞单层模型的细胞毒性研究证实了细胞周期分析的结果。在多种细胞系中,与对照和单独治疗相比,联合治疗的细胞毒性显著提高。NCI/ADR-RES 癌细胞球体进一步证明了 NCL-240/2-DG 组合的有效性。