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升高的BCRP转运器和改变的NF-kB通路在MCF-7细胞中介导着索莱德龙酸抵抗

Öykü Irmak Dikkatli^1,2, Yunus Emre Cavlak^1,3, Yaprak Dönmez Çakıl⁴

¹Department of Molecular Biology and Genetics, Institute of Science, Başkent University, Ankara, Türkiye.

Journal of biochemical and molecular toxicology

|July 14, 2025

概括

乳腺癌细胞中索莱德龙酸耐药性涉及增加的人类乳腺癌耐药性蛋白 (BCRP) 和改变NF-κB信号传递. 这种抵抗机制不涉及表皮层-介质细胞过渡 (EMT) 标志物.

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:

双酸盐Zoledronic acid (ZA) 是癌症骨保存的标准治疗方法.
通过NF-κB等细胞内信号通路,ZA具有抗癌作用,抑制增殖并诱导亡.
对ZA的获得性耐药性构成了重大的临床挑战.

研究的目的:

研究MCF-7乳腺癌细胞中ZA耐药性的机制.
检查人类乳腺癌抗性蛋白 (BCRP) 和NF-κB通路在ZA耐药性中的作用.
评估ZA耐药细胞中的上皮层-介质细胞过渡 (EMT) 标记物.

主要方法:

MCF-7细胞被逐步选择以抵抗ZA,从而产生MCF-7/Zol细胞.
分析了BCRP的表达和局部化.
评估了NF-κB通路激活 (酸化IκB,核转移).
在家长细胞和耐药细胞中评估了EMT标记物.

主要成果:

MCF-7/Zol细胞显示BCRP水平升高,细胞内局部发生变化.
增加的BCRP活性导致抵抗性细胞中基质积累的减少.
抗ZA细胞显示酸化IκB和核NF-κB转位的增加.
在MCF-7/Zol细胞中没有观察到EMT标记物的显著变化.

结论:

提高BCRP的调节和激活NF-κB通路是MCF-7乳腺癌细胞中ZA抵抗的关键机制.
通过BCRP介导的流量和NF-κB信号传递有助于ZA耐药性.
在这个模型中,EMT不是ZA电阻的主要机制.
了解这些耐药性机制对于开发克服耐药性的策略和识别多药性耐药性 (MDR) 生物标志物至关重要.

关键词:

在ABCG2传送器上.在EMT中,EMT是EMT.通过NF-κB路径.佐勒多尼酸是一种酸.多种药物耐药性多种药物耐药性

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