TY - JOUR
T1 - Inhibition of nuclear factor-κB activity is involved in E1A mediated sensitization of radiation-induced apoptosis
AU - Shao, Ruping
AU - Karunagaran, Devarajan
AU - Zhou, Binhua P.
AU - Li, Kaiyi
AU - Lo, Su Shun
AU - Deng, Jiong
AU - Chiao, Paul
AU - Hung, Mien Chie
PY - 1997/12/26
Y1 - 1997/12/26
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0031466397&partnerID=8YFLogxK
U2 - 10.1074/jbc.272.52.32739
DO - 10.1074/jbc.272.52.32739
M3 - Article
C2 - 9407046
AN - SCOPUS:0031466397
SN - 0021-9258
VL - 272
SP - 32739
EP - 32742
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 52
ER -