Au(NHC) and Au(NHC), a monocarbene gold(I) complex and the corresponding bis(carbene) complex, are two structurally related compounds, endowed with cytotoxic properties against several cancer cell lines. Herein, we explore the molecular and cellular mechanisms at the basis of their cytotoxicity in A2780 human ovarian cancer cells. Through a comparative proteomic analysis, we demonstrated that the number of modulated proteins is far larger in Au(NHC)-treated than in Au(NHC)-treated A2780 cells.
View Article and Find Full Text PDFHere we present original data related to the research paper entitled "Proteome analysis in dystrophic mdx mouse muscle reveals a drastic alteration of Key Metabolic and Contractile Proteins after chronic exercise and the potential modulation by anti-oxidant compounds" (Gamberi et al., 2018) [1]. The dystrophin-deficient mdx mouse is the most common animal model for Duchenne muscular dystrophy.
View Article and Find Full Text PDFUnlabelled: Weakness and fatigability are typical features of Duchenne muscular dystrophy patients and are aggravated in dystrophic mdx mice by chronic treadmill exercise. In the present study, we describe, the pattern of differentially abundant spots that is associated to the worsening of dystrophy phenotype induced by chronic exercise. Our proteomic analysis pointed out 34 protein spots with different abundance between sedentary and exercised mdx mice.
View Article and Find Full Text PDFThe cellular alterations produced in cisplatin-resistant A2780 ovarian cancer cells (A2780/R) upon treatment with the cytotoxic organogold(III) complex Aubipyc were investigated in depth through a classical proteomic approach. We observed that A2780/R cell exposure to a cytotoxic concentration of Aubipyc for 24 hours results in a conspicuous number of alterations at the protein level that were carefully examined. Notably, we observed that several affected proteins belong to the glucose metabolism system further supporting the idea that the cytotoxic effects of Aubipyc in A2780/R cells are mostly mediated by an impairment of glucose metabolism in excellent agreement with previous observations on the parent cisplatin-sensitive cell line.
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