Figure 3.

Schematic illustration of the pathways linking NF-κB to cellular senescence, cancer, and aging.

Notes: Inflammation, DNA damage, and oxidative/oncogenic stress all lead to the activation of IKKα/IKKβ resulting in the activation of NF-κB. NF-κB can inhibit tumorigenesis and promote aging by inducing a senescence growth arrest and SASP. Alternatively, depending upon the signal, NF-κB may promote tumorigenesis by activating cell cycle progression, blocking apoptosis, and inducing SASP for example.

Abbreviations: ATM, ataxia telangiectasia mutated kinase; CIP, cyclin dependent kinase interacting protein; CDK, cyclin dependent kinase; CycD, cyclin D; DNA, deoxyribonucleic acid; EGFR, epidermal growth factor receptor; FOXO, forkhead box; IGF1R, insulin like growth factor 1 receptor; HMGB1, high mobility group protein B1; IKK, IkB kinase; IL, interleukin; IR, insulin receptor; MAPK, mitogen activated protein kinase; miRNA, micro ribonucleic acid; NEMO, NF-kappa B essential modulator, also known as inhibitor of nuclear factor kappa B kinase subunit gamma; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; Pi3K, phosphatidylinositol 3-kinase; PIP, phosphatidylinositol phosphate; pRB, retinoblastoma protein; SASP, senescence associated secretory phenotype; TAB, transforming growth factor-beta activated kinase binding protein; TAK, transforming growth factor-beta activated kinase; TGF, transforming growth factor; TNF, tumor necrosis factor; TRAFS, TNF receptor associated factors.