Regulation of Akt by EGF-R inhibitors, a possible mechanism of EGF-R inhibitor-enhanced TRAIL-induced apoptosis

• Published in: Biochemical and biophysical research communications Vol. 295; no. 2; pp. 515 - 518
• Main Authors: Park, Sang-Youel, Seol, Dai-Wu
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 12.07.2002
• Subjects: Akt; Apoptosis; Apoptosis - drug effects; Apoptosis - physiology; Apoptosis Regulatory Proteins; Cell Line; EGF-R; ErbB Receptors - antagonists & inhibitors; Genistein; Genistein - pharmacology; Membrane Glycoproteins - physiology; Phosphorylation; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins - drug effects; Proto-Oncogene Proteins - physiology; Proto-Oncogene Proteins c-akt; Pyrimidines - pharmacology; Quinazolines - pharmacology; Recombinant Proteins - metabolism; TNF-Related Apoptosis-Inducing Ligand; TRAIL; Tumor Necrosis Factor-alpha - physiology; TRAIL; Akt; EGF-R; Genistein; Apoptosis

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a type II transmembrane cytokine and a potent inducer of apoptosis. Epidermal growth factor (EGF) signaling is well known to involve in tumor survival and overexpression of EGF receptor (EGF-R) attributes to decreased responsiv...