1. ¹Department of Surgery, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
2. ²Department of Biology, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
3. ³Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA

Correspondence: AS Baldwin, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Mason Farm Rd, Chapel Hill, NC 27599-7295, USA. Tel: 919 966 3652; Fax: 919 966 0444; E-mail: abaldwin@med.unc.edu

Received 8 November 2005; Revised 22 December 2005; Accepted 9 January 2006; Published online 17 February 2006.

Abstract

The transcription factor NF-B and associated regulatory factors (including IB kinase subunits and the IB family member Bcl-3) are strongly implicated in a variety of hematologic and solid tumor malignancies. A role for NF-B in cancer cells appears to involve regulation of cell proliferation, control of apoptosis, promotion of angiogenesis, and stimulation of invasion/metastasis. Consistent with a role for NF-B in oncogenesis are observations that inhibition of NF-B alone or in combination with cancer therapies leads to tumor cell death or growth inhibition. However, other experimental data indicate that NF-B can play a tumor suppressor role in certain settings and that it can be important in promoting an apoptotic signal downstream of certain cancer therapy regimens. In order to appropriately move NF-B inhibitors in the clinic, thorough approaches must be initiated to determine the molecular mechanisms that dictate the complexity of oncologic and therapeutic outcomes that are controlled by NF-B.