PMID: 11606372Oct 19, 2001Paper

E1A inhibition of radiation-induced NF-kappaB activity through suppression of IKK activity and IkappaB degradation, independent of Akt activation

Cancer Research
R ShaoM C Hung

Abstract

Activation of the transcription factor nuclear factor kappaB (NF-kappaB) has been implicated in the protection of cells from apoptosis. We have shown previously that the adenovirus type 5 E1A sensitizes cells to radiation-induced apoptosis by inhibiting NF-kappaB activity. However, the exact mechanism of inhibition is not known. In this study, we compared the activity of inhibitor of nuclear factor-kappaB (IkappaB) kinase (IKK) and the degradation of IkappaBalpha in E1A transfectants and parental human cancer cells after ionizing radiation treatment. We found that radiation-induced IKK activity and IkappaBalpha degradation were inhibited in the E1A transfectants. Recently, Akt has been implicated in NF-kappaB activation. To test whether Akt is regulated by E1A and is involved in radiation-induced NF-kappaB activity, we examined the phosphorylation status of Akt in the E1A transfectants and parental cells and in irradiated cells. The results indicated that radiation induced Akt phosphorylation and that E1A inhibited basal but not radiation-induced Akt phosphorylation. We additionally examined radiation-induced NF-kappaB activity in cells stably transfected with a dominant-negative, inactive Akt and in parental cancer cells treat...Continue Reading

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