L-2 Selenium and selenoproteins in redox signaling

Publication date: July 2017
Source:Free Radical Biology and Medicine, Volume 108, Supplement 1
Author(s): Anna P. Kipp
The European population is only suboptimally supplied with the essential trace element selenium. Different selenium species either modify the cellular redox status directly or have indirect effects after incorporation into selenoproteins. In the past years, we have been working on the role of glutathione peroxidases such as GPx2. In addition, consequences of a suboptimal selenium status have been studied in mice indicating that redox-regulated pathways including Nrf2, Wnt, and NF-kB are modified under such conditions. Especially the up-regulation of antioxidant Nrf2 target genes might be an attempt to compensate for the reduced expression of selenoproteins. It is well accepted that cancer cells are characterized by substantial differences in maintaining and regulating their redox status in comparison to normal cells. Cancer cells highly depend on antioxidant enzymes and thus profit from a high selenium supply. On the contrary, a suboptimal selenium status increases the risk to develop a tumor. Depending on the tumor model, also GPx2 can act anti- and pro-carcinogenic. Using a 3D culture model, we started to elucidate which cell types within multicellular spheroids have a high basal and inducible activity of redox-regulated transcription factors. Based on that, we aim to understand better, how redox signaling and thus the selenium status contribute to tumorigenesis.



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