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Proteasome activation is critical for cell death induced by inhibitors of polo-like kinase 1 (PLK1) in multiple cancers.

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成果类型:
期刊论文
作者:
Wang, Yufei;Wang, Guihua;Xiang, Wei;Liu, Xueting;Jiang, Manli;...
通讯作者:
Hu, Jinyue
作者机构:
[Wang, Yufei; Xiang, Wei; Jiang, Manli; Liu, Xueting] Medical Research Center, Affiliated Changsha Central Hospital of Hengyang Medical School, University of South China, Changsha, 410004, China
[Wang, Guihua] Department of Oncology, Affiliated Changsha Central Hospital of Hengyang Medical School, University of South China, Changsha, 410004, China
[Hu, Jinyue] Medical Research Center, Affiliated Changsha Central Hospital of Hengyang Medical School, University of South China, Changsha, 410004, China. Electronic address: 2018050703@usc.edu.cn
通讯机构:
[Hu, Jinyue] M
Medical Research Center, Affiliated Changsha Central Hospital of Hengyang Medical School, University of South China, Changsha, 410004, China. Electronic address:
语种:
英文
关键词:
BI2536;Cancer;Cell death;GW843682X;PLK1;Proteasome
期刊:
European Journal of Pharmacology
ISSN:
0014-2999
年:
2024
卷:
972
页码:
176558
机构署名:
本校为第一且通讯机构
摘要:
Inhibitors of polo-like kinase (PLK) are currently being evaluated as anticancer drugs. However, the molecular mechanism of PLK inhibitor-induced cell death is not fully understood. In this study, we found that GW843682X and BI2536, two inhibitors of PLK1, significantly induced cell death in multiple type cells. The induction of cell death was related to the preferring expression of PLK1. However, in human umbilical vascular endothelial cells (HUVEC) and human colorectal carcinoma cells, which expressed higher levels of both PLK1 and PLK2, PLK1 inhibitors induced very low levels of cell death....

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