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A new Schiff base copper(II) complex induces cancer cell growth inhibition and apoptosis by multiple mechanisms

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机构: [1]School of Chemical Science and Technology, Yunnan University, Kunming 650091, Yunnan, China [2]Department of Chemical Biology and Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics (Theranostics), School of Pharmacy, Tianjin Medical University, Tianjin 300070, China [3]Biobank, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, Health Science Center, 518035 Shenzhen, China [4]Laboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, Kunming 650500, China [5]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China
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关键词: Schiff base Cu(II) complex Apoptosis Ubiquitination c-Myc and KLF5

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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 mu M, 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 (Kruppel-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.

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出版当年[2020]版:
大类 | 3 区 生物
小类 | 3 区 生化与分子生物学 3 区 无机化学与核化学
最新[2023]版:
大类 | 2 区 化学
小类 | 1 区 无机化学与核化学 3 区 生化与分子生物学
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出版当年[2019]版:
Q1 CHEMISTRY, INORGANIC & NUCLEAR Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
最新[2023]版:
Q1 CHEMISTRY, INORGANIC & NUCLEAR Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2019版] 出版当年五年平均 出版前一年[2018版] 出版后一年[2020版]

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第一作者机构: [1]School of Chemical Science and Technology, Yunnan University, Kunming 650091, Yunnan, China
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