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阻断PGE2诱导的瘤再生,可以消除膀癌的化学抵抗

Antonina V Kurtova¹, Jing Xiao², Qianxing Mo³

¹1] Department of Molecular &Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [2] Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.

|December 4, 2014

概括

膀癌的化疗耐药性是由癌症干细胞 (CSCs) 驱动的,它们在周期之间重新填充瘤. 通过阻断前列腺素E2 (PGE2) 信号传递,塞莱科克西布可以抑制这种CSC重组,从而可能提高化疗的有效性.

科学领域:

在瘤学瘤学.
癌症干细胞生物学
药物耐药性机制药物耐药性机制

背景情况:

化疗最初可以消除瘤,但可能导致逐渐不响应.
众所周知,癌症干细胞 (CSCs) 在化疗后因增强生存能力而被丰富.
驱动化学抵抗的精确机制,特别是CSC重新填充,需要进一步阐明.

研究的目的:

研究膀癌干细胞 (CSCs) 中治疗耐药性的新机制.
探索CSC增殖和前列腺素E2 (PGE2) 信号在化学抵抗中的作用.
评估向PGE2信号的潜力,作为膀泌尿细胞癌的辅助疗法.

主要方法:

利用人类膀癌异种移植来研究化疗后的CSC行为.
分析了静止CSCs在细胞分裂中的招募,以应对化疗.
研究了前列腺素E2 (PGE2) 和循环氧基因酶-2 (COX2) 在中枢神经细胞重组中的作用.
在体内给予COX2抑制剂赛莱科西布,以评估其对抗化学性能的影响.

主要成果:

化疗诱导膀中枢细胞在治疗周期之间繁殖和重新填充残留瘤.
化疗诱导的亡会释放PGE2,这在悖论上促进了CSC的重新繁殖.
通过中和抗体或 Celecoxib 废除的 CSC 重组阻断 PGE2 信号.
在体内给予赛莱科克西布,减弱了化学阻力,并消除了PGE2/COX2介导的伤口反应特征.

结论:

膀CSC通过类似于伤口修复的增殖反应,积极促进化疗抵抗.
PGE2信号传递在中介这种CSC重组和随后的化学抵抗方面发挥着至关重要的作用.
针对PGE2/COX2通路使用诸如赛莱科西布之类的药物,是克服膀泌尿道癌的化学抵抗的有前途的辅助策略.

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