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联合使用伊立替康和 p53 激活剂增强间皮瘤细胞的生长抑制作用。

Combined use of irinotecan and p53 activator enhances growth inhibition of mesothelioma cells.

机构信息

Department of Molecular Pathogenesis, Juntendo University Graduate School of Medicine, Tokyo, Japan.

Department of Biochemistry, Juntendo University Graduate School of Medicine, Tokyo, Japan.

出版信息

FEBS Open Bio. 2020 Nov;10(11):2375-2387. doi: 10.1002/2211-5463.12985. Epub 2020 Oct 5.

Abstract

Malignant mesothelioma (MM) is an aggressive malignant neoplasm which rapidly invades pleural tissues and has a poor prognosis. Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM. The level of CES2 mRNA was greatly increased on treatment with nutlin-3a. A combination of CPT-11 and nutlin-3a inhibited the growth of MM cells more effectively than either drug alone. Knocking down CES2 in MM cells reduced the effect of the drug combination, and its forced expression in MESO4 cells enhanced the growth inhibitory activity of CPT-11 in the absence of nutlin-3a. Enhancement of the growth inhibitory activity of CPT-11 by nutlin-3a suggests a possible new combinatorial MM chemotherapy regimen.

摘要

恶性间皮瘤(MM)是一种侵袭性恶性肿瘤,迅速侵袭胸膜组织,预后不良。在这里,我们通过 p53 依赖性诱导细胞溶质酯酶 2(CES2)来探索伊立替康(喜树碱-11(CPT-11))的效果增强,CES2 是一种 CPT-11 激活酶,在 MM 中。用 nutlin-3a 处理后,CES2 mRNA 的水平大大增加。CPT-11 和 nutlin-3a 的联合治疗比单独使用任何一种药物更有效地抑制 MM 细胞的生长。在 MM 细胞中敲低 CES2 会降低药物组合的效果,而在没有 nutlin-3a 的情况下,其在 MESO4 细胞中的强制表达增强了 CPT-11 的生长抑制活性。nutlin-3a 增强 CPT-11 的生长抑制活性表明可能有新的组合性 MM 化疗方案。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b76d/7609812/a52a21145075/FEB4-10-2375-g001.jpg

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