Katarzyna Gałczyńska , Aneta Węgierek-Ciuk , Katarzyna Durlik-Popińska , Paulina Żarnowiec , Krystyna Kurdziel , Michał Arabski
{"title":"铜(II)配合物与1-烯丙咪唑通过减弱Wnt、JAK-STAT和TGF-β信号通路诱导G2/M细胞周期阻滞,抑制A549癌细胞生长","authors":"Katarzyna Gałczyńska , Aneta Węgierek-Ciuk , Katarzyna Durlik-Popińska , Paulina Żarnowiec , Krystyna Kurdziel , Michał Arabski","doi":"10.1016/j.jinorgbio.2024.112791","DOIUrl":null,"url":null,"abstract":"<div><div>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)<sub>4</sub>(NO<sub>3</sub>)<sub>2</sub>] 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-β 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.</div></div>","PeriodicalId":364,"journal":{"name":"Journal of Inorganic Biochemistry","volume":"264 ","pages":"Article 112791"},"PeriodicalIF":3.8000,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"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\",\"authors\":\"Katarzyna Gałczyńska , Aneta Węgierek-Ciuk , Katarzyna Durlik-Popińska , Paulina Żarnowiec , Krystyna Kurdziel , Michał Arabski\",\"doi\":\"10.1016/j.jinorgbio.2024.112791\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>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)<sub>4</sub>(NO<sub>3</sub>)<sub>2</sub>] 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-β 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.</div></div>\",\"PeriodicalId\":364,\"journal\":{\"name\":\"Journal of Inorganic Biochemistry\",\"volume\":\"264 \",\"pages\":\"Article 112791\"},\"PeriodicalIF\":3.8000,\"publicationDate\":\"2024-11-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Inorganic Biochemistry\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0162013424003167\",\"RegionNum\":2,\"RegionCategory\":\"化学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Inorganic Biochemistry","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0162013424003167","RegionNum":2,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
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
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-β 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.
期刊介绍:
The Journal of Inorganic Biochemistry is an established international forum for research in all aspects of Biological Inorganic Chemistry. Original papers of a high scientific level are published in the form of Articles (full length papers), Short Communications, Focused Reviews and Bioinorganic Methods. Topics include: the chemistry, structure and function of metalloenzymes; the interaction of inorganic ions and molecules with proteins and nucleic acids; the synthesis and properties of coordination complexes of biological interest including both structural and functional model systems; the function of metal- containing systems in the regulation of gene expression; the role of metals in medicine; the application of spectroscopic methods to determine the structure of metallobiomolecules; the preparation and characterization of metal-based biomaterials; and related systems. The emphasis of the Journal is on the structure and mechanism of action of metallobiomolecules.