The causal relationship between
inflammation and
cancer has been documented for sometime, but its molecular nature remains ill defined. Increasing evidence suggested that inflammatory microenvironment in and around
tumors is an indispensable participant in the neoplastic process. High level of
free radicals produced during
inflammation significantly induces DNA damage while evading apoptosis, a hallmark of
cancer, reduces the capability of tissues to eliminate damaged cells. Therefore, the mechanism by which
inflammation affects the apoptosis pathway is crucial to understand
inflammation-associated
carcinogenesis. Nuclear factor-κB (NF-κB), a transcriptional factor, plays an important role in the regulation of inflammatory responses. NF-κB signaling, which can be activated by diverse stimuli including proinflammatory
cytokines, infectious agents and cellular stresses, has been shown to involve in
carcinogenesis and resistance to multiple
drug therapy. In this review, we focus on the role of NF-κB signaling on the apoptotic effect in
inflammation-associated
carcinogenesis. These insights may help us to consider the role of NF-κB in
inflammation and
cancer and further on as a target of drugs for the prevention and treatment of these diseases.