Effect of NF-kappa B Signaling on Apoptosis in Chronic Inflammation-Associated Carcinogenesis

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-kappa B (NF-kappa B), a transcriptional factor, plays an important role in the regulation of inflammatory responses. NF-kappa B signaling, which can be activated by diverse stimuli including proinflammatory cytokines, infectious agents and cellular stresses, has been shown to be involved in carcinogenesis and resistance to multiple drug therapy. In this review, we focus on the role of NF-kappa B signaling on the apoptotic effect in inflammation-associated carcinogenesis. These insights may help us to consider the role of NF-kappa B in inflammation and cancer and further on as a target of drugs for the prevention and treatment of these diseases.