通过阻断TFEB/FTH1信号传递,PTPRC可以抑制骨肉瘤细胞的铁亡
1Jingzhou Hospital Affiliated to Yangtze University, No.26 Chuyuan Avenue, Jingzhou District, Jingzhou City, 434020, Hubei Province, China. shaoyan.st@yangtzeu.edu.cn.
Molecular biotechnology
|October 18, 2023
概括
蛋白氨酸酸酶受体C型 (PTPRC) 通过抑制TFEB促进骨髓瘤 (OS),导致溶酶体生物发生和铁亡减少. 针对PTPRC/TFEB/FTH1可能为OS提供新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 蛋白氨酸酸酶受体C型 (PTPRC) 在各种癌症中具有致癌作用.
- 关于PTPRC在骨髓瘤 (OS) 中的作用存在有限的研究.
研究的目的:
- 探索PTPRC在骨髓瘤中的潜在作用和机制.
主要方法:
- 对于PTPRC表达的RT-qPCR和西部斑.
- lysosome生物发生的免疫光.
- 路西法酶和ChIP对TFEB-FTH1相互作用进行了测试.
- 细胞死亡的PI和TUNNEL染色.
主要成果:
- 在OS组织和细胞中,PTPRC过度表达.
- PTPRC的淘汰促进了TFEB酸化和核转位,增强了溶酶体生物发生和Fe2+积累.
- PTPRC的淘汰诱导了自,降低了FTH1/FTL的调节,并促进了依赖TFEB的铁亡.
结论:
- 通过TFEB介导的 lysosome生物发生和FTH1/FTL信号的调节,PTPRC Knockdown促进OS细胞铁亡.
- PTPRC/TFEB/FTH1通路代表了骨髓瘤的潜在治疗标.
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