Tumour cell uptake of the metastasis inhibitor ruthenium complex NAMI-A and its in vitro effects on KB cells

Abstract

These findings suggest the interaction of NAMI-A with biological components resulting in possible consequences for the distribution of the compound itself. Furthermore, NAMI-A enters tumour cells both by passive diffusion and by active transportation.

Cytotoxicity of half sandwich ruthenium(II) complexes with strong hydrogen bond acceptor ligands and their mechanism of action

“…Consequently, several attempts are being taken to develop inhibitors of metastases [50]. Moreover, ruthenium complexes with antimetastasis properties have been reported [51,52]. In order to test the antimetastatic ability of R5 and R6, we tested the ability of these two complexes to inhibit invasion by breast cancer cell line MDA-MB-231 cells.…”

Free Exchange across Cells, and Echistatin-Sensitive Membrane Target for the Metastasis Inhibitor NAMI-A (Imidazoliumtrans-Imidazole Dimethyl Sulfoxide Tetrachlororuthenate) on KB Tumor Cells

“…An established KB cell line, derived from a human epidermal carcinoma (European Collection of Cell Cultures number 86103004) was cultured as previously described (Frausin et al, 2002). The cell population doubling time was ca.…”

Preliminary chemico-biological studies on Ru(III) compounds with S-methyl pyrrolidine/dimethyl dithiocarbamate

“…Both in vitro and in vivo results seem to exclude DNA as the primary target for NAMI-A, whose DNA binding is much weaker than platinum complexes [15,21,22]. On the other hand, KP1019 was proved to induce apoptosis in colorectal tumor cell lines through the mitochondrial death pathway, and DNA might be a target, although studies have shown that KP1019 and cisplatin induce different types of DNA lesions [12,23].…”