Quiescin/sulfhydryl oxidase 1b (QSOX1b) induces migration and proliferation of vascular smooth muscle cells by distinct redox pathways.

Quiescent and contractile VSMC can switch to proliferative and migratory phenotype in response to growth factors and cytokines, an effect underscored by Nox family NADPH oxidases, particularly Nox1. We previously showed that quiescin/sulfhydryl oxidase 1 (QSOX1) has a role in neointima formation in balloon-injured rat carotid. Here, we investigated the intracellular redox mechanisms underlying these effects in primary VSMC.

Reactivity of dinuclear copper(II) complexes towards melanoma cells: Correlation with its stability, tyrosinase mimicking and nuclease activity.

In this work, the influence of two new dinuclear copper(II) complexes in the viability of melanoma cells (B16F10 and TM1MNG3) was investigated, with the aim of verifying possible correlations between their cytotoxicity and their structure. One of the complexes had a polydentate dinucleating amine-imine ligand (complex 2), and the other a tridentate imine and a diamine-bridging ligand (complex 4). The analogous mononuclear copper(II) species (complexes 1 and 3, respectively) were also prepared for comparative studies.

The flavo-oxidase QSOX1 supports vascular smooth muscle cell migration and proliferation: Evidence for a role in neointima growth.

Quiescin sulfhydryl oxidase 1 (QSOX1) is a flavoenzyme largely present in the extracellular milieu whose physiological functions and substrates are not known. QSOX1 has been implicated in the regulation of tumor cell survival, proliferation and migration, in addition to extracellular matrix (ECM) remodeling. However, data regarding other pathophysiological conditions are still lacking.

De novo galectin-3 expression influences the response of melanoma cells to isatin-Schiff base copper (II) complex-induced oxidative stimulus.

Galectin-3, a ubiquitous member of the galectin family, has been shown to control cellular proliferation, adhesion, migration and apoptosis; thus, it has a role in tumor development and progression. Galectin-3 expression is both up- and down-regulated during melanoma progression. However, conflicting data regarding its roles in tumor biology prompted us to investigate if the presence of galectin-3 influences the response of melanoma cells to a novel metallodrug because metastatic melanoma acquires chemo resistance and is reported to be redox-sensitive.