Peng Liang, Linghu Ruixia, Chen Demeng, Yang Jing, Kou Xiaoxue, Wang Xiang-Zhen, Hu Yi, Jiang Yi-Zhou, Yang Junlan
Oncology Department, Chinese PLA General Hospital, Beijing, China.
School of Dentistry, University of California Los Angeles, Los Angeles, CA, USA.
Exp Mol Med. 2017 Apr 21;49(4):e318. doi: 10.1038/emm.2017.15.
Esophageal squamous cell carcinoma (ESCC) is a deadly malignancy with regard to mortality and prognosis, and the 5-year survival rate for all patients diagnosed with ESCC remains poor. A better understanding of the biological mechanisms of ESCC tumorigenesis and progression is of great importance to improve treatment of this disease. In this study, we demonstrated that the glutathione metabolism pathway is highly enriched in ESCC cells compared with normal esophageal epithelial cells in an in vivo mouse model. In addition, treatment with L-buthionine-sulfoximine (BSO) to deplete glutathione decreased the ESCC tumor burden in mice, thus demonstrating the critical role of glutathione metabolism in ESCC progression. BSO treatment also led to decreased cell proliferation and activation of cell apoptosis in ESCC. Finally, BSO treatment blocked NF-kB pathway activation in ESCC. Our study reveals a new pathway that regulates ESCC progression and suggests that inhibition of glutathione metabolism may be a potential strategy for ESCC treatment.
食管鳞状细胞癌(ESCC)在死亡率和预后方面是一种致命的恶性肿瘤,所有被诊断为ESCC的患者5年生存率仍然很低。更好地了解ESCC肿瘤发生和进展的生物学机制对于改善这种疾病的治疗至关重要。在本研究中,我们证明,在体内小鼠模型中,与正常食管上皮细胞相比,ESCC细胞中谷胱甘肽代谢途径高度富集。此外,用L-丁硫氨酸-亚砜胺(BSO)处理以耗尽谷胱甘肽可减轻小鼠的ESCC肿瘤负担,从而证明谷胱甘肽代谢在ESCC进展中的关键作用。BSO处理还导致ESCC细胞增殖减少和细胞凋亡激活。最后,BSO处理阻断了ESCC中NF-κB途径的激活。我们的研究揭示了一条调节ESCC进展的新途径,并表明抑制谷胱甘肽代谢可能是ESCC治疗的一种潜在策略。