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Volume 272, Number 52, Issue of December 26, 1997 pp. 32739-32742
B Activity Is Involved in
E1A-mediated Sensitization of Radiation-induced Apoptosis
(Received for publication, August 5, 1997, and in revised form, October 5, 1997)
,
,
,
,
,
,
and
From the 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
Department of Tumor Biology,
Department of Surgical Oncology, The
University of Texas M. D. Anderson Cancer Center,
Houston, Texas 77030
-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-
B (NF-B) has been shown to
play a key role in the anti-apoptotic pathway of radiation-induced
apoptosis. In an attempt to determine whether NF-B was involved in
the E1A-mediated sensitization of radiation-induced apoptosis, we found
that radiation-induced activation of NF-B occurred in the parental
cells but was blocked in the E1A transfectants. Furthermore, parental
cells cotransfected with NF-B and E1A were better protected from
undergoing apoptosis upon irradiation than those transfected with E1A
alone. Thus, our results suggest that inhibition of NF-B activation
by E1A is a plausible mechanism for E1A-mediated sensitization of
radiation-induced apoptosis.
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