Engagement of PI-3-kinase mediated Protein kinase C ζ activation in protecting Friend cells from ionizing radiation-induced apoptosis
- Authors:
- Published online on: January 1, 2003 https://doi.org/10.3892/ijo.22.1.129
- Pages: 129-135
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Abstract
Murine erythroleukemia cells (Friend) respond to ionizing radiation with the activation and nuclear translocation of p85α subunit of phosphatidylinositol-3-kinase (PI-3-kinase) which mediates the downstream activation and nuclear translocation of atypical Protein kinase C ζ (PKC ζ). This event occurs mainly upon high dose of ionizing radiation (15 Gy) and is concomitant to an increase in BrdU incorporation, which probably accounts for a predominant repair DNA synthesis. Following treatment with wortmannin, a relatively specific inhibitor of PI-3-kinase, both an increased number of apoptotic cells and the inhibition of protein kinase C ζ translocation were detected. Altogether the evidence suggests a potential role of the PI-3-kinase/PKC ζ pathway in protecting Friend cells from ionizing radiation-induced apoptosis offering PKC ζ for consideration as possible target of pharmacological treatments.
