Copper(II) complex with 1-allylimidazole induces G2/M cell cycle arrest and suppresses A549 cancer cell growth by attenuating Wnt, JAK-STAT, and TGF-β signaling pathways

被引：0
|
作者：
Galczynska, Katarzyna [1 ]
Wegierek-Ciuk, Aneta [1 ]
Durlik-Popinska, Katarzyna [1 ]
Zarnowiec, Paulina [1 ]
Kurdziel, Krystyna [2 ]
Arabski, Michal [1 ]
机构：
[1] Jan Kochanowski Univ, Inst Biol, Uniwersytecka 7, PL-25406 Kielce, Poland
[2] Jan Kochanowski Univ, Inst Chem, Uniwersytecka 7, PL-25406 Kielce, Poland
来源：
JOURNAL OF INORGANIC BIOCHEMISTRY | 2025年 / 264卷
关键词：
Copper(II) complex; Anti-tumor activity; Apoptosis; ROS production; DNA damage; WNT pathway inhibition; IN-VITRO; DNA-BINDING; MIXED CHELATE; SCHIFF-BASE; X-RAY; APOPTOSIS; CU(II); PROLIFERATION; CYTOTOXICITY; GENOTOXICITY;
D O I：
10.1016/j.jinorgbio.2024.112791
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The main aim of the study was to investigate the molecular mechanism of action of the potentially anti-cancer agent copper(II) complex with 1-allylimidazole [Cu(1-allim)4(NO3)2] using the A549 lung cancer line, toward which it is selectively cytotoxic. Gene expression analysis showed that the complex caused apoptosis through WNT, JAK-STAT, and TGF-beta pathways. The complex induced DNA damage, ROS production, and depolarization of the mitochondrial membrane, suggesting that its toxicity is likely due to induction of the intrinsic apoptosis pathway. It also arrested the cell cycle at G2/M phase. Particularly noteworthy is that it inhibited the WNT pathway, a target for lung cancer therapies. Its complex mechanism of action may hinder the acquisition of immunity by cancer cells.
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页数：9
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