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Advances in Brief |
B Activation1
Departments of Surgery [J. C. C.] and Biology [A. S. B.], Lineberger Comprehensive Cancer Center [J. C. C., R. L., A. S. B.], Curriculum in Genetics and Molecular Biology [A. S. B], University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7210
Limited studies have indicated that some chemotherapy agents activate
the transcription factor nuclear factor-
B (NF-B), and that this
leads to suppression of the apoptotic potential of the chemotherapy. In
contrast, it was reported recently that stable inhibition of NF-B in
four different cancer cell lines did not lead to augmentation of the
chemotherapy-induced apoptosis. In this study, we have focused on
colorectal cancer, which is known to be highly resistant to genotoxic
chemotherapy and gamma irradiation. We show that the topoisomerase I
inhibitor
7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin
(CPT-11) activates NF-B in most colorectal cancer cell lines. We
then examine a therapeutic strategy that uses adenovirus-mediated
transfer of the super-repressor IB
to inhibit NF-B activation
as an adjuvant approach to promote chemosensitivity in colorectal tumor
cells to treatment with CPT-11. These data demonstrate that the
protection from apoptosis induced in response to CPT-11 treatment is
effectively inhibited by the transient inhibition of NF-B in a
variety of human colon cancer cell lines and in a tumor xenograft
model, resulting in a significantly enhanced tumoricidal response to
CPT-11 via increased induction of apoptosis. These findings indicate
that the activation of NF-B by chemotherapy is an important
underlying mechanism of inducible chemoresistance.
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