【摘 要】
：
The death receptor TNFR1 induces apoptosis in many tissues upon cross-linking by its ligand (TNF-α)and cotreatment with a protein synthesis inhibitor, cycloheximide, but a number of cancer cells resis
【机 构】
：
Pharmacology Research Center,Shanghai Medical College,Fudan University,Shanghai 200032,China
【出 处】
：
International Conference for Physiological Sciences 2012(201
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The death receptor TNFR1 induces apoptosis in many tissues upon cross-linking by its ligand (TNF-α)and cotreatment with a protein synthesis inhibitor, cycloheximide, but a number of cancer cells resistant to such apoptosis.Recently G-protein-coupled receptor kinases (GRKs),which are an importantfamily of Ser/Thr kinases that specifically phosphorylate anddesensitize the activated GPCR, were found capable of phosphorylating nonreceptor substrates, such as p53 and Iκ Bα.In this study, we down-regulated GRKx expression in MDA-MB-231 cells by lentivirus, anddetermined the cell survival after treated with or without TNF-a by MTS assay.We found GRKx knockdown enhanced TNF-α-induced apoptosis, and we further determined this sensitization wasdue to inhibition ofNF-κB signalingafter GRKx knockdown.Thus, our study reveals a novel anticancer property of GRKx inhibition.
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