Serine protease inhibitors interact with IFN-γ through up-regulation of FasR; a novel therapeutic strategy against cancer
作者： Natalia Shadrin , Michal Glickman Shapira , Boris Khalfin , Lakshminarasaiah Uppalapati , Abraham H. Parola
DOI: 10.1016/J.YEXCR.2014.11.005
关键词: Fas receptor 、 HeLa 、 Molecular biology 、 Cell 、 Programmed cell death 、 Proteases 、 Protease 、 Biology 、 Serine 、 Elastase inhibitor
摘要: Abstract Among the many immunomodulatory and anti-tumor activities, IFN-γ up-regulates tumor cell death mediated by Fas receptor (FasR). Our several other studies have demonstrated involvement of trypsin-like proteases (TLPs) in mode action IFN-γ. In present study, we tried to unravel role serine induced Fas-mediated death. results show that both tosyl- l -Lysine chloromethylketone (TLCK), a trypsin like protease inhibitor -phenylalanine (TPCK) – chymotrypsin (CLP) inhibitor, sensitize HeLa cells The combined effect these inhibitors with anti-Fas was stronger than additive. contrast, elastase III (EI), which also contains chloromethyl ketone moiety, not active. Furthermore, co-addition TLCK or TPCK markedly enhanced Fas-induced led up-regulation FasR on its own, further TPCK. This evident increased expression surface elevated mRNA level. study may provide basis for design novel combinatory therapeutic strategy could enhance eradication tumors.
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