acetyl-aspartyl-glutamyl-valyl-aspartal and Sarcoma

Hepatocyte growth factor, which is now known to be the same protein as scatter factor, induced oligonucleosomal fragmentation of nuclear DNA of Sarcoma 180 cells and increased the activity of caspase-3, a key component in control of the apoptotic cell death pathway to about 2.6 times that in control cells on 48 hr incubation, but did not increase the activity of caspase-1. Both HGF-induced DNA fragmentation and caspase-3 activity were completely inhibited by co-incubation with an inhibitor of caspase-3, Ac-DEVD-H. In contrast, HGF did not affect the expression of the apoptosis suppressors Bcl-2 and Bcl-x. These results indicate that HGF activates the apoptosis signaling pathway by increasing caspase-3 activity in Sarcoma 180 cells.

Topics: Animals; Apoptosis; bcl-X Protein; Caspase 1; Caspase 3; Caspases; Cell Survival; Cysteine Endopeptidases; DNA Fragmentation; Enzyme Activation; Enzyme Inhibitors; Gene Expression Regulation, Neoplastic; Hepatocyte Growth Factor; Mice; Neoplasm Proteins; Oligopeptides; Proto-Oncogene Proteins c-bcl-2; Sarcoma; Signal Transduction; Suppression, Genetic; Tumor Cells, Cultured