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化合物 C 通过阻断细胞周期进程、黏附和侵袭抑制同基因小鼠模型中的 Renca 肾上皮癌生长。

Compound C Inhibits Renca Renal Epithelial Carcinoma Growth in Syngeneic Mouse Models by Blocking Cell Cycle Progression, Adhesion and Invasion.

机构信息

Department of Medicine, Gachon University School of Medicine, Incheon 21999, Korea.

Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999, Korea.

出版信息

Int J Mol Sci. 2022 Aug 26;23(17):9675. doi: 10.3390/ijms23179675.

DOI:10.3390/ijms23179675
PMID:36077072
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9456023/
Abstract

Compound C (CompC), an inhibitor of AMP-activated protein kinase, reduces the viability of various renal carcinoma cells. The molecular mechanism underlying anti-proliferative effect was investigated by flow cytometry and western blot analysis in Renca cells. Its effect on the growth of Renca xenografts was also examined in a syngeneic BALB/c mouse model. Subsequent results demonstrated that CompC reduced platelet-derived growth factor receptor signaling pathways and increased ERK1/2 activation as well as reactive oxygen species (ROS) production. CompC also increased the level of active Wee1 tyrosine kinase (P-Ser-Wee1) and the inactive form of Cdk1 (P-Tyr-Cdk1) while reducing the level of active histone H3 (P-Ser-H3). ROS-dependent ERK1/2 activation and sequential alterations in Wee1, Cdk1, and histone H3 might be responsible for the CompC-induced G2/M cell cycle arrest and cell viability reduction. In addition, CompC reduced the adhesion, migration, and invasion of Renca cells in the in vitro cell systems, and growth of Renca xenografts in the BALB/c mouse model. Taken together, the inhibition of in vivo tumor growth by CompC may be attributed to the blockage of cell cycle progression, adhesion, migration, and invasion of tumor cells. These findings suggest the therapeutic potential of CompC against tumor development and progression.

摘要

化合物 C（CompC）是一种 AMP 激活的蛋白激酶抑制剂，可降低各种肾癌细胞的活力。通过流式细胞术和 Western blot 分析在 Renca 细胞中研究了其抗增殖作用的分子机制。在同基因 BALB/c 小鼠模型中还检查了 CompC 对 Renca 异种移植物生长的影响。随后的结果表明，CompC 降低了血小板衍生生长因子受体信号通路，并增加了 ERK1/2 激活和活性氧（ROS）的产生。CompC 还增加了活性 Wee1 酪氨酸激酶（P-Ser-Wee1）和失活形式的 Cdk1（P-Tyr-Cdk1）的水平，同时降低了活性组蛋白 H3（P-Ser-H3）的水平。ROS 依赖性 ERK1/2 激活以及随后的 Wee1、Cdk1 和组蛋白 H3 的改变可能是 CompC 诱导的 G2/M 细胞周期停滞和细胞活力降低的原因。此外，CompC 降低了体外细胞系统中 Renca 细胞的黏附、迁移和侵袭以及 BALB/c 小鼠模型中 Renca 异种移植物的生长。总之，CompC 抑制体内肿瘤生长可能归因于阻断肿瘤细胞的细胞周期进程、黏附、迁移和侵袭。这些发现表明 CompC 具有针对肿瘤发展和进展的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e46/9456023/f3cb4b8d60ea/ijms-23-09675-g009.jpg
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