National Cancer Research Center, Department of Experimental Pharmacology, Serbia.
Anticancer Agents Med Chem. 2012 Nov;12(9):1071-80. doi: 10.2174/187152012803529682.
Our previous studies showed that zinc (II), cadmium (II) and nickel (II) complexes with 2-formylpyridine selenosemicarbazone induce apoptosis in cancer cells via activation of mitochondrial pathway. Herein, we reported their antimetastatic properties. Nickel (II), and zinc (II) complexes exhibited the strongest inhibitory potential towards MMP-2/9, while all investigated compounds significantly decreased proteolytic activity of MMP-2/9 in human breast cancer MDA-MB-361 cells. As shown by in vitro transmembrane assays, nickel (II) complex was the most effective in inhibiting invasion of MDA-MB-361 cells, while the cadmium (II) complex was the most active in inhibiting HeLa cells invasion. In malignant cells, the complexes inhibited intracellular accumulation of reactive oxygen species, known for its pro-angiogenic properties via VEGF signaling, but no reduction in total cellular amount of VEGF was found. Furthermore, tubulogenesis test showed anti-angiogenic effect of the complexes in treated endothelial cells. Data indicate multiple mechanisms of the complexes' anti-angiogenic properties. In addition, they could modulate metastatic phenotype of tumor cells. Nickel (II) complex with 2-formylpyridine selenosemicarbazone revealed to be the most potent.
我们之前的研究表明,2-甲酰基吡啶硒代缩氨基脲的锌(II)、镉(II)和镍(II)配合物通过激活线粒体途径诱导癌细胞凋亡。在此,我们报告了它们的抗转移特性。镍(II)和锌(II)配合物对 MMP-2/9 表现出最强的抑制潜力,而所有研究的化合物均显著降低了人乳腺癌 MDA-MB-361 细胞中 MMP-2/9 的蛋白水解活性。如体外跨膜测定所示,镍(II)配合物在抑制 MDA-MB-361 细胞侵袭方面最有效,而镉(II)配合物在抑制 HeLa 细胞侵袭方面最活跃。在恶性细胞中,这些配合物抑制了活性氧的细胞内积累,活性氧通过 VEGF 信号具有促血管生成特性,但未发现 VEGF 的总细胞含量减少。此外,管状形成试验显示了复合物在处理的内皮细胞中的抗血管生成作用。数据表明了复合物抗血管生成特性的多种机制。此外,它们还可以调节肿瘤细胞的转移表型。具有 2-甲酰基吡啶硒代缩氨基脲的镍(II)配合物被证明是最有效的。