Abstract
Nuclear Factor-kappa B (NF-κB) is a transcription factor family that regulates a large number of genes that are involved in important physiological processes, including survival, inflammation, and immune responses. More recently, constitutive expression of NF-κB has been associated with several types of cancer. In addition, microorganisms, such as viruses and bacteria, cooperate in the activation of NF-κB in tumors, confirming the multifactorial role of this transcription factor as a cancer driver. Recent reports have shown that the NF-κB signaling pathway should receive attention for the development of therapies. In addition to the direct effects of NF-κB in cancer cells, it might also impact immune cells that can both promote or prevent tumor development. Currently, with the rise of cancer immunotherapy, the link among immune cells, inflammation, and cancer is a major focus, and NF-κB could be an important regulator for the success of these therapies. This review discusses the contrasting roles of NF-κB as a regulator of pro- and antitumor processes and its potential as a therapeutic target.
Highlights
Laboratório de Célula-Tronco, Instituto Nacional de Câncer, 20230-130 Rio de Janeiro, RJ, Brazil; These authors contributed to this article
Its activation occurs in the ventral region of the egg when the receptor toll binds to the ligand spätzle, which triggers signal transduction that culminates in the destruction of cactus, which is an inhibitory protein that binds to dorsal in the cytoplasm
In vitro co-cultures of macrophages and tumor cells not always support the role of tumor cells promoting an anti-inflammatory phenotype of macrophages
Summary
Tumor cells cells can can secrete secrete anti-inflammatory anti-inflammatory factors, factors, rendering rendering macrophages macrophages aa tumor tumor supportive supportive phenotype, phenotype, known known as as tumor tumor associated macrophages (TAMs). In. In vitro co-cultures of macrophages and tumor cells not always support the role of tumor cells promoting an anti-inflammatory phenotype of macrophages. In vitro co-cultures of macrophages and tumor cells not always support the role of tumor cells promoting an anti-inflammatory phenotype of macrophages It seems that different tumors can induce different phenotypes on macrophages, macrophages, even promoting its antitumor activity, throughNF-κB. Numerous data have indicated a positive feedback between NF-κB activation and inflammatory signaling that favors tumor development, such as the up-regulation of cyclooxigenase (COX)-2; nitric oxide synthase (NOS); inflammatory cytokines, such as IL-6, IL-8, and TNF-α; and, chemokines, such as CCL2 and CXCL8 [9,69]. We discuss the specific role of NF-κB in different types of neoplasia
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