赛可沙宁-D通过准PIM1/c-Myc轴来触发癌细胞死亡,从而重新编程致癌的替代拼接

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Xin Zhang¹, Xuehui Li^2,3, Feng Zhang⁴

¹Department of Gastrointestinal Surgery, Second Affiliated Hospital of Naval Medical University, Shanghai, China.

Cell death discovery

|October 6, 2025

概括

赛可沙宁D (SSD) 通过向PIM1/Myc通路,显示出强大的抗瘤作用. 这种机制重新连接了癌症特异性的替代拼接,为各种癌症提供了新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

来自Radix Bupleuri的saikosaponins (SSs) 是具有潜在抗瘤特性的生物活性化合物.
具体的抗瘤机制和个别SSS的疗效,包括赛科萨松D (SSD),仍然在很大程度上未被描述.

研究的目的:

研究SSD在各种癌症类型中的抗瘤功效和潜在的分子机制.
阐明SSD在调节替代拼接中的作用及其与关键癌症相关蛋白质的相互作用.

主要方法:

在体内和体外癌症模型被用于评估SSD的抗瘤活性.
机理学研究涉及调查SSD的直接目标,蛋白质与蛋白质相互作用 (PIM1/Myc) 以及对替代拼接因子的影响.
使用CRISPR-Cas13和小分子抑制剂验证PIM1/Myc轴和SSD调节的替代拼接事件.

主要成果:

在体内和体外,SSD在各种癌症类型中表现出显著的抗瘤疗效.
发现SSD直接向PIM1,抑制PIM1-Myc相互作用并降低Myc酸化和稳定性.
这一有针对性的行动导致了Myc治理的替代拼接因子的下调,并重新连接致癌的替代拼接事件.

结论:

通过PIM1/Myc信号轴调节替代拼接,SSD表现出强大的抗瘤活性.
针对PIM1/Myc途径或SSD调节的替代拼接产品可以克服癌细胞和患者衍生器官 (PDO) 中对SSD治疗的抗性.
这些发现凸显了SSD作为有前途的抗癌剂,并揭示了癌症治疗的新治疗轴.

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