M Ołdak , J Malejczyk
Published:
GICID: 01.3001.0000.3220
Available language versions: en pl
Issue: Postepy Hig Med Dosw 1999; 53 (2)
Abstract
Stimulation of epidermal growth factor receptor (EGFR) leads to cell proliferation and plays an important role in cancerogenesis. It seems that these effects are a consequence of triggering of various signal transduction pathways involving PI-3K and MAP kinase activation. Surprisingly, under certain circumstances stimulation of EGFR may also result in cell growth arrest and apoptosis induction. It is possible that anti-proliferative effect of EGF depends on STAT protein activation. It has been reported, that STAT upregulates expression of cyclin-dependent kinase inhibitor, which blocks the cell cycle. Additionally, STAT may increase caspase 1 (ICE) expression, which seems to be necessary for apoptosis induced by EGF. Intracellular mechanisms involved in EGFR proapoptotic activity still remains poorly understood and, because of their potential clinical significance, require further investigation.