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超强增强剂驱动的SOX4/SMAD3通过调节脂代谢以加速白血病进展来调整中间膜重塑

Enzhe Lou^1,2, Peilong Lai³, Guanjie Peng⁴

¹Sino-French Hoffmann Institute, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|February 21, 2026

概括

新的研究确定SOX4和SMAD3是晚期慢性髓性白血病 (CML) 爆发阶段的关键驱动因素. 针对这些因素的Bemcentinib显示出治疗这种侵袭性白血病的前景.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

慢性髓性白血病 (CML) 爆发期 (BP) 由于治疗耐药性和生存率差,存在重大治疗挑战.
表观遗传变化和异常转录因子激活与癌症进展有关,但它们在CML-BP过渡中的作用尚未完全理解.

研究的目的:

研究特定的转录机制,推动CML从慢性阶段 (CP) 到爆发阶段 (BP) 的进展.
确定CML-BP的关键监管因素和潜在的治疗目标.

主要方法:

在CML-BP中识别超增强剂驱动的转录因子.
功能性测试,以评估已识别的因素在白血病进展中的作用.
对下游信号通路和分子相互作用的分析.
针对性治疗的体外和体外测试.

主要成果:

超增强剂驱动的SOX4和SMAD3被确定为CML-BP的关键调节剂.
SOX4和SMAD3之间的正反循环促进了白血病的进展.
SOX4/SMAD3轴增强了AXL受体氨酸激酶转录和信号传递.
通过SOX4/SMAD3对LPCAT1进行上调,有助于AXL的局部化.
AXL抑制剂贝姆森丁尼布在抑制CML-BP进展方面表现出有效性.

结论:

SOX4和SMAD3是CML-BP中的关键调节剂,由超级增强剂驱动.
SOX4/SMAD3-AXL信号轴是CML-BP进展的一个关键机制.
贝姆森提尼布代表了对CML-BP的有前途的治疗策略.

关键词:

爆炸阶段的爆发阶段慢性骨髓性白血病慢性骨髓性白血病超级增强剂超级增强剂有针对性的治疗方法.转录因子的转录因子

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