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| EWSR1-FLI1通过代谢重编程影响尤文肉瘤发生发展的研究进展 |
| 赵薇1,2,江润益2,江爱民3,龚海熠2,魏海峰2* |
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(1. 上海理工大学健康科学与工程学院, 上海 200093;
2. 海军军医大学(第二军医大学)第二附属医院骨肿瘤科, 上海 200003;
3. 海军军医大学(第二军医大学)第一附属医院泌尿外科, 上海 200433
*通信作者) |
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| 摘要: |
| 尤文肉瘤是发生于儿童和青少年的第二常见恶性原发性骨肿瘤，该病恶性程度极高，患者病程短，转移事件发生快，严重危害儿童和青少年的健康。肿瘤细胞通过一系列复杂的调控机制促进包括糖、氨基酸、脂类等在内的营养物质发生代谢重编程，进而维持肿瘤高代谢状态，促进肿瘤发生、发展；同时代谢重编程相关产物可作用于肿瘤微环境中各细胞组分，抑制肿瘤免疫反应，甚至诱导耐药事件的发生。尤文肉瘤断裂区域1（EWSR1）-佛氏白血病病毒整合蛋白1（FLI1）融合蛋白是尤文肉瘤的关键促癌分子，具有多重功能和复杂的调控机制，了解EWSR1-FLI1对尤文肉瘤细胞代谢变化的影响及其相关调控机制，可为探究尤文肉瘤的病因、寻找有效的诊疗靶点及治疗策略提供线索。本文就EWSR1-FLI1影响尤文肉瘤代谢重编程的相关研究进展进行汇总与剖析，旨在为该病的早期诊断和精准治疗提供新的思路。 |
| 关键词: 骨软骨瘤 尤文肉瘤 代谢重编程 EWSR1-FLI1 |
| DOI：10.16781/j.CN31-2187/R.20230415 |
| 投稿时间：2023-07-21修订日期：2023-09-13 |
| 基金项目:国家自然科学基金（82072971）. |
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| EWSR1-FLI1 affects the development and progression of Ewing’s sarcoma through metabolic reprogramming: research progress |
| ZHAO Wei1,2,JIANG Runyi2,JIANG Aimin3,GONG Haiyi2,WEI Haifeng2* |
(1. School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai 200093, China;
2. Department of Orthopaedic Oncology, The Second Affiliated Hospital of Naval Medical University (Second Military Medical University), Shanghai 200003, China;
3. Department of Urology, The First Affiliated Hospital of Naval Medical University (Second Military Medical University), Shanghai 200433, China
* Corresponding author) |
| Abstract: |
| Ewing’s sarcoma is the second most common malignant primary bone tumor in children and adolescents, marked by its exceptional malignancy, abbreviated patient course, and rapid metastasis, posing a substantial threat to the health of children and adolescents. Tumor cells promote metabolic reprogramming of nutrients including sugars, amino acids, lipids, and more through a series of complex regulatory mechanisms, thus maintaining the high metabolic state of tumor and promoting tumor development. The products related to metabolic reprogramming exert a significant impact on various cellular constituents in the tumor microenvironment, inhibiting anti-tumor immune responses, and even inducing drug resistance events. A pivotal player in this context is the Ewing sarcoma breakpoint region 1 (EWSR1)-Friend leukemia virus integration 1 (FLI1) fusion protein, which assumes multifaceted roles with intricate regulatory mechanisms. Understanding the specific metabolic changes and regulatory pathways orchestrated by EWSR1-FLI1 in Ewing’s sarcoma cells holds the promise of shedding light on the disease’s etiology. Additionally, this knowledge offers a path to the discovery of novel diagnostic and therapeutic markers and strategies. This article summarizes and analyzes the recent research progress of EWSR1-FLI1 on metabolic reprogramming in Ewing’s sarcoma, providing new ideas for the early diagnosis and precise treatment of the disease. |
| Key words: osteochondroma Ewing’s sarcoma metabolic reprogramming EWSR1-FLI1 |
