Gao Yanmei, Wang Chenxu, Liu Guobin, Zhang Ruilin, Ren Xuelian, Hu Guangyuan, Mei Qi, Huang He
State Key Laboratory of Chemical Biology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
School of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing 210023, China.
J Proteome Res. 2025 Sep 1. doi: 10.1021/acs.jproteome.5c00424.
Glioma is an aggressive brain tumor that requires challenging treatments. Tumor Treating Fields (TTFields), an FDA-approved therapy for glioblastoma (GBM), pleural mesothelioma, and platinum-refractory metastatic nonsmall cell lung cancer (in combination with PD-1/PD-L1 inhibitors or docetaxel), employs specific frequency electric fields to disrupt cell division and enhance treatment efficacy. However, their molecular mechanisms remain unclear. This study aimed to elucidate these mechanisms and optimize the therapeutic potential of TTFields through quantitative proteomics, phosphoproteomics, and glycoproteomics. Pathway analysis of the proteomics revealed that TTFields impact the cell cycle, DNA repair, autophagy, and DNA replication. Phosphoproteomic studies further demonstrated a marked decline in the activity of key kinases ABL1 and PDK1, while glycoproteomics highlighted disruptions in cell adhesion and ECM-receptor interactions. Notably, proteomic analysis identified an upregulation of PARP1 and BRD4 protein levels, suggesting a previously unrecognized resistance mechanism. Consistently, combining TTFields with inhibitors targeting these proteins significantly enhanced the treatment efficacy in U87 cells. Thus, this study uncovers comprehensive molecular mechanisms underlying TTFields' effects on GBM cells and supports the development of concomitant therapies to enhance treatment efficacy.
胶质瘤是一种侵袭性脑肿瘤,需要具有挑战性的治疗方法。肿瘤治疗电场(TTFields)是一种经美国食品药品监督管理局(FDA)批准用于治疗胶质母细胞瘤(GBM)、胸膜间皮瘤和铂类难治性转移性非小细胞肺癌(与PD-1/PD-L1抑制剂或多西他赛联合使用)的疗法,它利用特定频率的电场来破坏细胞分裂并提高治疗效果。然而,其分子机制仍不清楚。本研究旨在通过定量蛋白质组学、磷酸化蛋白质组学和糖蛋白质组学阐明这些机制,并优化TTFields的治疗潜力。蛋白质组学的通路分析表明,TTFields会影响细胞周期、DNA修复、自噬和DNA复制。磷酸化蛋白质组学研究进一步证明关键激酶ABL1和PDK1的活性显著下降,而糖蛋白质组学则突出了细胞黏附以及细胞外基质-受体相互作用的破坏。值得注意的是,蛋白质组学分析发现PARP1和BRD4蛋白水平上调,这表明存在一种先前未被认识的耐药机制。一致地,将TTFields与靶向这些蛋白质的抑制剂联合使用可显著提高对U87细胞的治疗效果。因此,本研究揭示了TTFields对GBM细胞作用的全面分子机制,并支持开发联合疗法以提高治疗效果。