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Department of Radiation Medicine, Division of Radiation Research, Georgetown University, Washington, District of Columbia

Requests for reprints: Mira Jung, Department of Radiation Medicine, Division of Radiation Research, Georgetown University, Research Building, Suite E211, Box 571482, Washington, DC 20057-1482. Phone: 202-687-8352; Fax: 202-687-7529. E-mail: jungm{at}georgetown.edu

The transcription factor nuclear factor-B (NF-B) is activated in response to various stimuli including ionizing radiation. Disruption of NF-B activation by mutant forms of the NF-B inhibitor IB- or by proteasome inhibitors enhances both sensitivity to radiation and radiation-induced apoptosis. Human squamous carcinoma SCC-35 cells stably expressing a fragment (residues 1 to 84) of human p65 have been shown to exhibit down-regulation of both endogenous p65 mRNA and its protein. The mutant protein also inhibited radiation-induced NF-B activation by preventing the proteolysis of IB-. This resulted in enhancement of cellular radiosensitivity and radiation-induced apoptosis. The NH₂-terminal region of p65 is thus a potential molecular target for disruption of NF-B activation and sensitization of tumors to radiotherapy.

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Note: Current address of K. Kim: AngioLab, Inc., Bio-Med RRC, Pai Chai University, Taejon, Korea.

Received 11/18/03; revised 3/24/04; accepted 4/13/04.