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ZBTB11消耗准K-Ras抑制剂耐药PDAC中的代谢漏洞

Nathan L Tran^1,2, Jiewei Jiang¹, Min Ma¹

¹Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, CA.

bioRxiv : the preprint server for biology

|June 3, 2024

概括

新的分子粘剂准ZBTB11,以克服胰腺癌中的K-Ras抑制剂耐药性. 这种方法选择性地耗尽癌细胞中的线粒体成分,提供了一个有前途的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
药物发现药物发现药物发现

背景情况:

胰腺管道腺癌 (PDAC) 经常含有K-Ras突变,导致通过代谢重编程对K-Ras抑制剂治疗产生抗性.
PDAC细胞中的耐药性将新陈代谢转向氧化酸化,这种状态易受线粒体复合物I抑制的影响,但由于神经毒性,这种状态耐受不良.

结论:

ZBTB11是对K-Ras抑制剂耐药PDAC的验证漏洞.
针对ZBTB11的分子降解剂为耐药胰腺癌提供了选择性的治疗策略.
这项工作为进一步调查ZBTB11在癌症代谢中的功能提供了有价值的工具化合物.

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