| Summary: | Persistent activation of the pro-inflammatory transcription factor nuclear factor-κB (NF-κB) is frequently observed in several human malignancies and can drive the processes of tumor initiation, oncogenic transformation, and malignant progression. Once activated, this master transcription factor regulates the expression of numerous genes involved in proliferation, survival, metastasis, angiogenesis, chemoresistance, and radioresistance. Thus, novel pharmacological agents that can suppress constitutive and/or inducible NF-κB activation have the potential for cancer therapy. In this review, we describe in detail the pleiotropic molecular mechanisms of aberrant NF-κB activation and also discuss various therapeutic strategies employed to suppress deregulated activation of this important oncogenic transcription factor in cancer.
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