The rare earth metal Gd(III), Yb(III), Lu(III), Eu(III), Tb(III) and Ho(III) complexes 1–6 with 2-((2-(pyridin-2-yl)hydrazono)methyl)quinolin-8-ol (H-L) as ligands were synthesized. The in vitro cytotoxicity assay indicated that the cytotoxicity of 1 was equivalent to cisplatin and higher than that of H-L and other complexes towards T24 tumor cells. The mechanism study indicated that 1 caused significant up-regulation of the proteins p27, p21 and p53 in T24 cells and cell cycle arrest in G2 phase. In addition, 1 induced effective T24 cells apoptosis via mitochondrial dysfunction pathway, which was indicated by changes in mitochondrial membrane potential (Δψ), reactive oxygen species (ROS), intracellular Ca²⁺ and the mitochondria-related proteins (including cytochrome C (Cyt C), B-cell lymphoma-2 (Bcl-2), Bcl-2-associated x (Bax) and apoptotic protease activating factor-1 (Apaf-1)). Moreover, 1 could activate caspase-3/8/9 in T24 cells. Therefore, complex 1 is a promising and potent anticancer drug candidate.

稀土类金属的Gd（III），镱（III），路（III），铕（III），铽（III）和Ho（III）配合物1 - 6 2 - （（2-（吡啶-2-基合成了作为配体的）（肼基）甲基）喹啉-8-醇（HL）。体外细胞毒性试验表明，1对T24肿瘤细胞的细胞毒性与顺铂相当，并且比HL和其他复合物更高。机制研究表明1引起T24细胞中p27，p21和p53蛋白的显着上调，并使细胞周期停滞在G2期。另外，1通过线粒体功能障碍途径诱导有效的T24细胞凋亡，其表现为线粒体膜电位（Δψ），活性氧（ROS），细胞内Ca ²⁺和线粒体相关蛋白（包括细胞色素C（Cyt C），B -细胞淋巴瘤2（Bcl-2），Bcl-2相关x（Bax）和凋亡蛋白酶激活因子1（Apaf-1））。此外，1可以激活T24细胞中的caspase-3 / 8/9。因此，复合物1是一种有前途和有效的抗癌药物候选物。