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.

合成了一种新的席夫碱铜（II）络合物[ N，N'-双（2'-羟基苯基丙酮）-邻乙二胺]铜（II）（M1），并通过单X射线晶体学对其进行了表征。通过MTT（3-（4,5-二甲基噻唑基-2-基）2,5-）评价复合物M1对HeLa，LoVo，A549，A549 / cis癌细胞系和正常细胞系LO2和HUVEC的细胞毒性。溴化二苯基四唑）测定法。IC ₅₀（50％抑制浓度）在5.13-11.68μM的范围内，基于铂摩尔浓度，它略低于顺铂。此外，抗癌机制研究表明，复合物M1通过阻止DNA合成来抑制细胞增殖，然后随着时间的推移作用于HeLa细胞的核分裂。此外，M1以剂量依赖的方式增加细胞内ROS（活性氧）的水平。蛋白质印迹分析表明，M1在HeLa中显着降低了c-Myc转录因子和KLF5（类Krüppel因子5）蛋白的表达水平。M1不抑制蛋白酶体活性。最后，M1诱导DNA损伤并激活DNA损伤修复途径。