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Research Article

塞来昔布和二甲基塞拉可昔阻断乳腺癌干细胞中的氧化磷酸化、上皮-间充质转化和侵袭性

卷 29, 期 15, 2022

发表于: 12 January, 2022

页: [2719 - 2735] 页: 17

弟呕挨: 10.2174/0929867328666211005124015

价格: $65

摘要

背景：成功治疗癌症的主要障碍是乳腺癌干细胞（BCSC）产生的耐药性和侵袭性。 目的：由于这两个过程具有高度的能量依赖性，因此确定干细胞活力所需的主要ATP供应者可能有助于设计新的治疗策略以预防恶性癌。 方法：通过评估BCSC中相关蛋白质含量、酶活性和通路通量，系统分析其能量代谢（糖酵解和氧化磷酸化、OxPhos）。一旦被确定为主要的ATP供应者，选择性能量抑制剂和规范的乳腺癌药物被用来阻断干细胞活力和转移特性。 结果：BCSC的OxPhos和糖酵解蛋白含量以及HK和LDH活性均比其亲本MCF-7细胞系高数倍。然而，BCSC中的CS，GDH，COX活性和两种能量代谢通量均显着低于MCF-7细胞（38-86%）。OxPhos是BCSC中主要的ATP提供者（>85%）。因此，寡霉素（一种特异性和有效的规范OxPhos抑制剂）和其他对OxPhos具有抑制作用的非规范药物（塞来昔布，二甲基西来昔布）显着降低了BCSC的活力，上皮 - 间充质转变蛋白的水平，侵入性和诱导的ROS过度产生，IC50值在24小时的治疗中范围为1至20μM。相比之下，糖酵解抑制剂（棉酚，碘乙酸，3-溴丙酮酸，2-脱氧葡萄糖）和规范化疗药物（紫杉醇，阿霉素，顺铂）对BCSC活力（IC50>100μM）的效果要差得多。 结论：这些结果表明，使用一些非甾体抗炎药可能是靶向BCSC的一种有前途的替代治疗策略。

关键词: 乳腺癌干细胞，塞来昔布，糖酵解，氧化磷酸化，紫杉醇，干细胞。

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