The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
South China University of Technology School of Medicine, Guangzhou, China.
Cell Death Dis. 2024 May 20;15(5):349. doi: 10.1038/s41419-024-06727-1.
Osteosarcoma is a malignant bone tumor that primarily inflicts the youth. It often metastasizes to the lungs after chemotherapy failure, which eventually shortens patients' lives. Thus, there is a dire clinical need to develop a novel therapy to tackle osteosarcoma metastasis. Methionine dependence is a special metabolic characteristic of most malignant tumor cells that may offer a target pathway for such therapy. Herein, we demonstrated that methionine deficiency restricted the growth and metastasis of cultured human osteosarcoma cells. A genetically engineered Salmonella, SGN1, capable of overexpressing an L-methioninase and hydrolyzing methionine led to significant reduction of methionine and S-adenosyl-methionine (SAM) specifically in tumor tissues, drastically restricted the growth and metastasis in subcutaneous xenograft, orthotopic, and tail vein-injected metastatic models, and prolonged the survival of the model animals. SGN1 also sharply suppressed the growth of patient-derived organoid and xenograft. Methionine restriction in the osteosarcoma cells initiated severe mitochondrial dysfunction, as evident in the dysregulated gene expression of respiratory chains, increased mitochondrial ROS generation, reduced ATP production, decreased basal and maximum respiration, and damaged mitochondrial membrane potential. Transcriptomic and molecular analysis revealed the reduction of C1orf112 expression as a primary mechanism underlies methionine deprivation-initiated suppression on the growth and metastasis as well as mitochondrial functions. Collectively, our findings unraveled a molecular linkage between methionine restriction, mitochondrial function, and osteosarcoma growth and metastasis. A pharmacological agent, such as SGN1, that can achieve tumor specific deprivation of methionine may represent a promising modality against the metastasis of osteosarcoma and potentially other types of sarcomas as well.
骨肉瘤是一种主要侵袭年轻人的恶性骨肿瘤。化疗失败后,它经常转移到肺部,最终缩短患者的生命。因此,迫切需要开发一种新的疗法来治疗骨肉瘤转移。甲硫氨酸依赖性是大多数恶性肿瘤细胞的一种特殊代谢特征,可能为这种治疗提供一个目标途径。在这里,我们证明了蛋氨酸缺乏限制了培养的人骨肉瘤细胞的生长和转移。一种能够过表达 L-甲硫氨酸酶并水解蛋氨酸的基因工程化沙门氏菌 SGN1 导致肿瘤组织中蛋氨酸和 S-腺苷甲硫氨酸(SAM)的显著减少,大大限制了皮下异种移植、原位和尾静脉注射转移模型中的生长和转移,并延长了模型动物的存活时间。SGN1 还明显抑制了患者来源的类器官和异种移植物的生长。骨肉瘤细胞中的蛋氨酸限制引发了严重的线粒体功能障碍,表现在呼吸链基因表达失调、线粒体 ROS 生成增加、ATP 产生减少、基础呼吸和最大呼吸减少以及线粒体膜电位受损。转录组学和分子分析揭示了 C1orf112 表达的减少是蛋氨酸剥夺引发的生长和转移以及线粒体功能抑制的主要机制。一种药理制剂,如 SGN1,能够实现肿瘤特异性蛋氨酸剥夺,可能代表一种有前途的治疗方法,用于治疗骨肉瘤转移,以及可能其他类型的肉瘤。