Publication: Anticancer applications of nanostructured silica-based materials functionalized with titanocene derivatives: Induction of cell death mechanism through TNFR1 modulation
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2018-01-31
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MDPI
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Abstract
A series of cytotoxic titanocene derivatives have been immobilized onto nanostructured silica-based materials using two different synthetic routes, namely, (i) a simple grafting protocol via protonolysis of the Ti-Cl bond; and (ii) a tethering method by elimination of ethanol using triethoxysilyl moieties of thiolato ligands attached to titanium. The resulting nanostructured systems have been characterized by different techniques such as XRD, XRF, DR-UV, BET, SEM, and TEM, observing the incorporation of the titanocene derivatives onto the nanostructured silica and slight changes in the textural features of the materials after functionalization with the metallodrugs. A complete biological study has been carried out using the synthesized materials exhibiting moderate cytotoxicity in vitro against three human hepatic carcinoma (HepG2, SK-Hep-1, Hep3B) and three human colon carcinomas (DLD-1, HT-29, COLO320) and very low cytotoxicity against normal cell lines. In addition, the cells' metabolic activity was modified by a 24-h exposure in a dose-dependent manner. Despite not having a significant effect on TNFalfa or the proinflammatory interleukin 1alfa secretion, the materials strongly modulated tumor necrosis factor (TNF) signaling, even at sub-cytotoxic concentrations. This is achieved mainly by upregulation of the TNFR1 receptor production, something which has not previously been observed for these systems.
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This article belongs to the Special Issue Nanomaterials for Biomedical Applications
Keywords
Nanostructured silica, Titanocene, Cytotoxicity, Anticancer, Tumor necrosis factor, Tnfr1 modulation
Bibliographic citation
Gómez-Ruiz, S., García-Peñas, A., Prashar, S., Rodríguez-Diéguez, A., & Fischer-Fodor, E. (2018). Anticancer Applications of Nanostructured Silica-Based Materials Functionalized with Titanocene Derivatives: Induction of Cell Death Mechanism through TNFR1 Modulation. Materials 11 (2), p. 224.