Inhibition of nuclear factor-κB activity is involved in E1A mediated sensitization of radiation-induced apoptosis

Ruping Shao, Devarajan Karunagaran, Binhua P. Zhou, Kaiyi Li, Su Shun Lo, Jiong Deng, Paul Chiao, Mien Chie Hung

Research output: Contribution to journalArticlepeer-review

115 Scopus citations

Abstract

The adenoviral E1A protein has been implicated in the potentiation of apoptosis induced by various external stimuli, but the exact mechanism of that potentiation is not clear. In this study, we compared the sensitivity to ionizing γ-irradiation of E1A transfectants with that of parental cells in a human ovarian cancer cell line (SKOV3.ip1); we found that the E1A transfectants became sensitive to radiation-induced apoptosis. Recently, activation of the transcription factor nuclear factor-κB (NF-κB) has been shown to play a key role in the anti-apoptotic pathway of radiation-induced apoptosis. In an attempt to determine whether NF-κB was involved in the E1A- mediated sensitization of radiation-induced apoptosis, we found that radiation-induced activation of NF-κB occurred in the parental cells but was blocked in the E1A transfectants. Furthermore, parental cells cotransfected with NF-κB and E1A were better protected from undergoing apoptosis upon irradiation than those transfected with E1A alone. Thus, our results suggest that inhibition of NF-κB activation by E1A is a plausible mechanism for E1A- mediated sensitization of radiation-induced apoptosis.

Original languageEnglish (US)
Pages (from-to)32739-32742
Number of pages4
JournalJournal of Biological Chemistry
Volume272
Issue number52
DOIs
StatePublished - Dec 26 1997

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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