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超增强剂驱动的MLX通过SLC7A11在骨髓瘤中调节氧化还原平衡的维持

Weitang Guo¹, Xin Wang², Bing Lu³

¹Department of Musculoskeletal Oncology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.

Cell death & disease

|July 17, 2023

概括

超强增强剂驱动的MLX蛋白通过调节代谢途径和铁运输来促进骨肉瘤的生长. 抑制MLX或准SLC7A11会诱导铁,为这种骨癌提供了一个有前途的治疗策略.

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:

骨肉瘤 (OS) 的治疗进展有限,超级增强剂在癌细胞转录成中发挥着至关重要的作用.
麦克斯样蛋白X (MLX) 是Myc-MLX网络的一部分,由超级增强剂驱动,其上调与OS预后差相关.

研究的目的:

调查MLX在骨髓瘤进展中的作用,并确定其下游目标和机制.
探索针对MLX或其相关途径用于骨髓瘤治疗的潜力.

主要方法:

在骨髓瘤细胞系和体内模型中对MLX的抑制.
转录组测序以识别MLX调节的途径.
铁代谢和铁灭诱导的分析.
关于MLX调节SLC7A11和谷氨 (GSH) 合成的研究.
评估硫沙拉对骨髓瘤生长的影响.

主要成果:

通过MLX的敲除,骨髓瘤的生长和转移受到了损害.
MLX调节了新陈代谢的重编程,包括脂质新陈代谢和铁素运输.
通过增加细胞铁素水平,MLX敲击诱导铁.
MLX积极调节谷氨酸/氨酸反载体SLC7A11,这对GSH生物合成和氧化还原平衡至关重要.
作为SLC7A11的抑制剂,sulfasalazine诱导了ferroptosis,并在体内抑制了瘤的生长.

结论:

超强增强剂驱动的MLX通过调节SLC7A11,氨酸吸收和氧化还原平衡来促进骨髓瘤.
针对SLC7A11的药物如硫沙是一种可行的和临床上有前途的治疗策略,用于骨髓瘤.

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