Friend erythroleukemia cells require high doses (15 Gy) of ionizing radiation to display a reduced rate of proliferation and an increased number of dead cells. Since ionizing radiation can activate several signaling pathways at the plasma membrane which can lead to the nuclear translocation of a number of proteins, we looked at the intranuclear signaling system activated by Protein Kinases C, being this family of enzymes involved in the regulation of cell growth and death. Our results show an early and dose-dependent increased activity of and 6 isoforms, although PKC is the only isoform significantly active and translocated into the nuclear compartment upon low (1.5 Gy) and high (15 Gy) radiation doses. These observations are concomitant and consistent with an increase in the anti-apoptotic protein Bcl-2 level upon both radiation doses. Our results point at the involvement of the PKC pathway in the survival response to ionizing radiation of this peculiar cell line, offering PKC C for consideration as a possible target of pharmacological treatments aimed at amplifying the effect of such a genotoxic agent. (C) 2002 Wiley-Liss, Inc.

Cataldi, A., Centurione, L., Di Pietro, R., Rapino, M., Bosco, D., Grifone, G., et al. (2003). Protein Kinase C zeta nuclear translocation mediates the occurrence of radioresistance in friend erythroleukemia cells. JOURNAL OF CELLULAR BIOCHEMISTRY, 88(1), 144-151 [10.1002/jcb.10305].

Protein Kinase C zeta nuclear translocation mediates the occurrence of radioresistance in friend erythroleukemia cells

GARACI, FRANCESCO;
2003-01-01

Abstract

Friend erythroleukemia cells require high doses (15 Gy) of ionizing radiation to display a reduced rate of proliferation and an increased number of dead cells. Since ionizing radiation can activate several signaling pathways at the plasma membrane which can lead to the nuclear translocation of a number of proteins, we looked at the intranuclear signaling system activated by Protein Kinases C, being this family of enzymes involved in the regulation of cell growth and death. Our results show an early and dose-dependent increased activity of and 6 isoforms, although PKC is the only isoform significantly active and translocated into the nuclear compartment upon low (1.5 Gy) and high (15 Gy) radiation doses. These observations are concomitant and consistent with an increase in the anti-apoptotic protein Bcl-2 level upon both radiation doses. Our results point at the involvement of the PKC pathway in the survival response to ionizing radiation of this peculiar cell line, offering PKC C for consideration as a possible target of pharmacological treatments aimed at amplifying the effect of such a genotoxic agent. (C) 2002 Wiley-Liss, Inc.
2003
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore MED/36 - DIAGNOSTICA PER IMMAGINI E RADIOTERAPIA
English
Con Impact Factor ISI
PKC zeta; radioresistance; friend cells
RADIATION-INDUCED APOPTOSIS; IONIZING-RADIATION; MESSENGER-RNA; ACTIVATION; ALPHA; TUMOR; EXPRESSION; LEUKEMIA; DELTA; PHOSPHORYLATION
Cataldi, A., Centurione, L., Di Pietro, R., Rapino, M., Bosco, D., Grifone, G., et al. (2003). Protein Kinase C zeta nuclear translocation mediates the occurrence of radioresistance in friend erythroleukemia cells. JOURNAL OF CELLULAR BIOCHEMISTRY, 88(1), 144-151 [10.1002/jcb.10305].
Cataldi, A; Centurione, L; Di Pietro, R; Rapino, M; Bosco, D; Grifone, G; Garaci, F; Rana, R
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/70310
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