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Da Eun Lee¹, Hae Min Lee¹, Yunhyeok Jun¹

¹School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu 41566, Republic of Korea.

Biochimica et biophysica acta. Molecular cell research

|November 5, 2024

概括

甲福明与与瘤亡因子 (TNF) 相关的亡诱导配体 (TRAIL) 结合,有效地克服结直肠癌 (CRC) 细胞中的化疗耐药性. 这种组合疗法诱导了显著的癌细胞死亡,为治疗耐 TRAIL 抗性 CRC 提供了一个有前途的策略.

科学领域:

在瘤学瘤学.
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

大肠直肠癌 (CRC) 通常会对化疗产生耐药性,导致复发和转移.
组合疗法对于克服耐药性和提高CRC治疗疗效至关重要.
与瘤亡因子 (TNF) 相关的诱导亡联体 (TRAIL) 是有前途的,但由于某些CRC细胞系的抗性而面临局限性,如SW620.

研究的目的:

为了研究甲福明和 TRAIL 对抗 TRAIL 的 SW620结直肠癌细胞的联合亡效应.
为了阐明底层的分子机制的协同作用抗癌活动的甲胺和TRAIL.

主要方法:

用甲福明和/或 TRAIL 治疗 SW620 CRC 细胞.
对亡诱导,酶激活和关键信号通路 (AKT/mTOR,NF-κB) 的分析.
评估内质网膜 (ER) 应激,CCAAT增强剂结合蛋白同类蛋白 (CHOP) 激活,以及细胞循环停止.
使用活体老鼠异种移植CRC模型进行验证.

主要成果:

单独使用 TRAIL 并不能诱导SW620细胞的亡,但与甲福明的联合治疗显著增强了亡.
甲胺通过抑制AKT/mTOR和NF-κB通路,降低X链系亡抑制剂 (XIAP) 水平,并诱导ER压力介导的CHOP激活来抵消 TRAIL耐药性.
甲胺还诱导了细胞循环的停止,抑制了癌细胞的增殖.
在体内研究证实,联合甲福明和 TRAIL 治疗导致瘤细胞死亡.

结论:

与甲福明和TRAIL联合治疗是一种有效的策略,可以诱导亡并克服结肠直肠癌中TRAIL的耐药性.
这种组合疗法显示出显著的抗癌效应,突出显示了其在耐 TRAIL 抗性 CRC 中临床应用的潜力.
了解甲胺和TRAIL之间的分子相互作用为开发结直肠癌的新疗法提供了基础.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.结肠直肠癌是一种癌症.压力ERER压力ERER压力甲胺是一种甲胺.在 NF-κBB 中.轨道的轨道是一个轨道.

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