Publication date: Available online 9 January 2018
Source:Free Radical Biology and Medicine
Author(s): Martin Bertz, Katrin Kühn, Solveigh C. Koeberle, Mike F. Müller, Doerte Hoelzer, Karolin Thies, Stefanie Deubel, René Thierbach, Anna P. Kipp
Selenoprotein H (SELENOH) is supposed to be involved in redox regulation as well as in tumorigenesis. However, its role in healthy and transformed cells of the gastrointestinal tract remains elusive. We analysed SELENOH expression in cells depending on their selenium supply and differentiation status and found that SELENOH expression was increased in tumor tissue, in undifferentiated epithelial cells from mice and in colorectal cancer lines as compared to more differentiated ones. Knockdown studies in human colorectal cancer cells revealed that repression of SELENOH decreased cellular differentiation and increased proliferation and migration. In addition, SELENOH knockdown cells have a higher competence to form colonies or tumor xenografts. In parallel, they show a faster cell cycle transition. The high levels of SELENOH in tumors as well as in undifferentiated, proliferative cells together with its inhibitory effects on proliferation and G1/S phase transition suggest SELENOH as a key regulator for cell cycle progression and for prevention of uncontrolled proliferation. As SELENOH expression is highly dependent on the selenium status, effects of selenium supplementation on cancer initiation and progression appear to involve SELENOH.
Graphical abstract
http://ift.tt/2mj440a
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου