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选择性但非泛CDK抑制取消了5FU驱动的组织因子在结肠癌中的上调

Annika Kayser¹, Annabell Wolff^1,2, Peggy Berlin³

¹Department of Medicine, Clinic III - Hematology, Oncology, Palliative Medicine, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany.

Scientific reports

|May 8, 2024

概括

化疗可以通过增加组织因子 (TF) 来诱导癌症的高凝血能力. 作为一种CDK抑制剂的Abemaciclib可以抵消这种作用,从而有可能在癌症患者中防止危险的血栓形成.

科学领域:

在瘤学瘤学.
血液学血液学血液学
药理学药理学是指药理学的学科.

背景情况:

血栓塞栓事件是癌症患者的重要并发症.
癌症中的高凝血性与组织因子 (TF) 途径有关,这是一个潜在的治疗点.

研究的目的:

研究化疗药物和循环林依赖性激酶抑制剂 (CDKI) 对结直肠癌细胞中TF表达和凝血的影响.
评估CDKIs,特别是abemaciclib在缓解化疗诱导的高凝血能力方面的潜力.

主要方法:

人类结直肠癌细胞 (HROC173) 用5-FU或凝替丁治疗,以诱导TF表达.
在单独和组合使用各种CDKIs (abemaciclib,palbociclib,THZ-1,dinaciclib) 治疗后,分析了细胞的TF丰度,上皮层-介质细胞过渡标志物和凝血潜力.
进行了功能凝血测试和TF抗体阻断实验.

主要成果:

低剂量化疗 (5-FU,gemcitabine) 诱导高凝血状态和显著上调TF,与上皮-介质细胞过渡相关.
迪纳西克利布和THZ-1提高了TF的调节,而阿贝马西克利布和帕尔博西克利布降低了TF的调节,并表现出抗凝剂活性.
阿贝马西克利布逆转了化疗诱导的TF上调和延长的凝血时间,独立于细胞毒性或衰老.

结论:

阿贝马西克利布通过降低TF的调节和抵消化疗引起的高凝血,显示出抗凝血特性.
在接受化疗的癌症患者中,短期的abemaciclib治疗可以预防血栓栓塞事件.
用特定的CDKI准TF途径为管理癌症相关血栓形成提供了一个有前途的策略.

关键词:

细胞分类细胞分类皮质 - 介质细胞过渡.过高凝血是一种高凝血.微小片是微小的片.衰老是一种衰老.有针对性的治疗.

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