A new Schiff base copper(II) complex induces cancer cell growth inhibition and apoptosis by multiple mechanisms
Copyright © 2020 Elsevier Inc. All rights reserved..
A new Schiff base copper(II) complex [N,N'-bis(2'-hydroxyphenylacetone)-o-ethanediamine] copper (II) (M1) has been synthesized and characterized by single X-ray crystallography. The cytotoxicity of complex M1 was evaluated against HeLa, LoVo, A549, A549/cis cancer cell lines, and the normal cell lines LO2 and HUVEC, by MTT (3-(4,5-dimethylthiazoyl-2-yl)2,5-diphenyltetrazoliumbromide) assays. The IC50 (50% inhibition concentrations) is in the range of 5.13-11.68 μM, which is somewhat lower than cisplatin on the basis of platinum molar concentration. Furthermore, anticancer mechanistic studies showed that the complex M1 inhibited cell proliferation by blocking DNA synthesis and then acted on nuclear division of HeLa cells over time. Moreover, M1 increased intracellular ROS (Reactive oxygen species) levels in a dose-dependent manner. Western blot analysis indicated M1 dramatically decrease c-Myc transcription factor and KLF5 (Krüppel-like factor 5) protein expression levels in HeLa. M1 did not inhibit proteasomal activity. Finally, M1 induced DNA damages and activated the DNA damage repair pathways.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2020 |
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Erschienen: |
2020 |
Enthalten in: |
Zur Gesamtaufnahme - volume:208 |
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Enthalten in: |
Journal of inorganic biochemistry - 208(2020) vom: 01. Juli, Seite 111103 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Bao, Rui-Dan [VerfasserIn] |
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Links: |
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Themen: |
789U1901C5 |
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Anmerkungen: |
Date Completed 08.06.2021 Date Revised 08.06.2021 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1016/j.jinorgbio.2020.111103 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM310845777 |
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520 | |a Copyright © 2020 Elsevier Inc. All rights reserved. | ||
520 | |a A new Schiff base copper(II) complex [N,N'-bis(2'-hydroxyphenylacetone)-o-ethanediamine] copper (II) (M1) has been synthesized and characterized by single X-ray crystallography. The cytotoxicity of complex M1 was evaluated against HeLa, LoVo, A549, A549/cis cancer cell lines, and the normal cell lines LO2 and HUVEC, by MTT (3-(4,5-dimethylthiazoyl-2-yl)2,5-diphenyltetrazoliumbromide) assays. The IC50 (50% inhibition concentrations) is in the range of 5.13-11.68 μM, which is somewhat lower than cisplatin on the basis of platinum molar concentration. Furthermore, anticancer mechanistic studies showed that the complex M1 inhibited cell proliferation by blocking DNA synthesis and then acted on nuclear division of HeLa cells over time. Moreover, M1 increased intracellular ROS (Reactive oxygen species) levels in a dose-dependent manner. Western blot analysis indicated M1 dramatically decrease c-Myc transcription factor and KLF5 (Krüppel-like factor 5) protein expression levels in HeLa. M1 did not inhibit proteasomal activity. Finally, M1 induced DNA damages and activated the DNA damage repair pathways | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 4 | |a Apoptosis | |
650 | 4 | |a Schiff base Cu(II) complex | |
650 | 4 | |a Ubiquitination | |
650 | 4 | |a c-Myc and KLF5 | |
650 | 7 | |a Antineoplastic Agents |2 NLM | |
650 | 7 | |a Coordination Complexes |2 NLM | |
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700 | 1 | |a Song, Xue-Qing |e verfasserin |4 aut | |
700 | 1 | |a Kong, Yan-Jie |e verfasserin |4 aut | |
700 | 1 | |a Li, Fang-Fang |e verfasserin |4 aut | |
700 | 1 | |a Liao, Wen-Hui |e verfasserin |4 aut | |
700 | 1 | |a Zhou, Jie |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Ji-Hong |e verfasserin |4 aut | |
700 | 1 | |a Zhao, Qi-Hua |e verfasserin |4 aut | |
700 | 1 | |a Xu, Jing-Yuan |e verfasserin |4 aut | |
700 | 1 | |a Chen, Ce-Shi |e verfasserin |4 aut | |
700 | 1 | |a Xie, Ming-Jin |e verfasserin |4 aut | |
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