study its role in tumor development [136, 137] and to sensitize tumor cells to apoptosis-inducing agents [134, 135]. Inhibiting NF-κB through the expression of an IκBα super-repressor (IκBαSR) has also been used to sensitize chemoresistant tumors to TNFα- and CPT-11-induced apoptosis, resulting in tumor regression [138], and to inhibit the proliferation of human head and neck carcinoma cells in vitro and in vivo [139]. However, IκBαSRs have also been shown to interact with and affect the activity of non-NF-κB pathway proteins including p53 [140], cyclin-dependent kinase 4 [141], and HDACs [142]. Furthermore, IκBαSR overexpression has been associated with the spontaneous development of squamous cell carcinoma in a murine model [143].
