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BRAFV600E/p-ERK/p-DRP1(Ser616) 促进瘤进展和重编程葡萄糖代谢在乳头甲状腺癌中的甲状腺癌
Shi-Shuai Wen1,2, Yi-Jun Wu1, Jia-Yang Wang3
1Department of Thyroid Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, P.R. China.
Thyroid : official journal of the American Thyroid Association
|August 20, 2024
概括
在乳头甲状腺癌中BRAFV600E突变驱动有氧糖解和通过BRAF/ERK/DRP1途径的进展. 与2-脱氧-D-葡萄糖 (2-DG) 和达布拉费尼布的联合治疗显示出对治疗BRAFV600E-阳性PTC的前景.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症新陈代谢 癌症新陈代谢
背景情况:
- 患有BRAFV600E突变的乳头甲状腺癌 (PTC) 的预后不佳,由于耐药性,BRAF抑制剂的有效性有限.
- 华堡效应在癌症中的作用及其与PTC中BRAFV600E的关联仍然不清楚.
研究的目的:
- 研究BRAFV600E和动相关蛋白1 (DRP1) 对PTC细胞过程,包括葡萄糖代谢的影响.
- 阐明BRAFV600E/DRP1监管相互作用及其在PTC进展中的作用.
- 为了评估2 - 脱氧 - D - 葡萄糖 (2-DG) 和达布拉费尼布联合治疗的疗效.
主要方法:
- 用RT-qPCR分析甲状腺癌组织中的糖溶性酶表达.
- 西方斑块和免疫组织化学研究BRAFV600E和DRP1的相互作用.
- 在体外和体内对BRAFV600E,DRP1和治疗干预措施的评估.
主要成果:
- BRAFV600E突变显著增加了有氧糖解,并减少了PTC中的氧化酸化.
- BRAFV600E/p-ERK/p-DRP1(Ser616) 途径上调六金酶2,增强细胞增殖,促进线粒体裂变,并降低ROS水平,抑制亡.
- 联合2-DG和dabrafenib治疗有效地抑制了BRAFV600E-阳性PTC的进展.
结论:
- BRAFV600E/p-ERK/p-DRP1(Ser616) 途径对于葡萄糖代谢重编程和BRAFV600E-阳性PTC中的积极进展至关重要.
- 通过联合2-DG和dabrafenib准这种途径提供了一个潜在的治疗策略,以改善BRAFV600E突变的PTC患者的结果.
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