Abstract
Protein kinase C (PKC) plays an important role in radiation-induced apoptosis. However, each function of PKC subtypes remains unclear. In this study, signaling pathways of radiation-induced activation of PKCδ were assessed in radiation-sensitive mouse thymic lymphomas. We have already demonstrated that PKCδ is an important regulator in the radiation-induced apoptosis in 3SBH5 cells, one of radiation-sensitive mouse thymic lymphomas. Indeed, PKCδ signal detected by Western blot in cytosols of 3SBH5 cells was outstandingly decreased after irradiation. In contrast, in XR223, the resistant cells derived from 3SBH5, the PKCδ signal in the cytosols was decreased very slightly. Interestingly, the signal of endogenous PKCδ in cytosols in XR223 was stronger than that in 3SBH5 cells. On the other hand, mouse thymic lymphoma cells derived from Atm null(-/-) mouse were radioresistant than those from Atm wild-type mouse in terms of apoptosis. Besides, degradation of PKCδ by irradiation was observed in Atm(+/+) cells but not in Atm(-/-) cells. However, there was no difference in the distribution of endogenous PKCδ between the two cell lines. The regulation of PKCδ distribution, which is presumably distinct from the AT-mediated cascade, may determine radiation sensitivity in 3SB lines(3SBH5 and XR223).
