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Updated: Aug 23, 2026

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells
Published on: June 9, 2020
The p65 subunit of nuclear factor-kappaB is a molecular target for radiation sensitization of human squamous
Kyoung M Kim1, Yin Zhang, Bo-Yeon Kim
1Department of Radiation Medicine, Division of Radiation Research, Georgetown University, Research Building, Suite E211, Box 571482, Washington, DC 20057-1482, USA.
Abstract:
The transcription factor nuclear factor-kappaB (NF-kappaB) is activated in response to various stimuli including ionizing radiation. Disruption of NF-kappaB activation by mutant forms of the NF-kappaB inhibitor IkappaB-alpha 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-kappaB activation by preventing the proteolysis of IkappaB-alpha. This resulted in enhancement of cellular radiosensitivity and radiation-induced apoptosis. The NH(2)-terminal region of p65 is thus a potential molecular target for disruption of NF-kappaB activation and sensitization of tumors to radiotherapy.
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