NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) is an important transcription factor involved in a variety of cellular processes relevant to cancer, including inflammation, immune responses, and cell survival. It plays a significant role in cancer development and progression by regulating the expression of many genes that are involved in cell proliferation, apoptosis resistance, angiogenesis, invasion, and metastasis. The NF-kB signalling pathway consists of a family of transcription factors, primarily composed of five subunits: p50, p52, p65 (RelA), RelB, and c-Rel. These subunits can form homodimers or heterodimers and are normally sequestered in the cytoplasm by inhibitors called IkBs (inhibitor of kappa B proteins). In response to various stimuli including cytokines, pathogens, or genotoxic stress, the NF-kB pathway is activated, leading to the degradation of IkBs through phosphorylation and ubiquitination, allowing the NF-kB subunits to translocate into the nucleus. Once in the nucleus, NF-kB binds to specific DNA sequences, known as κB sites (or NFκB response elements), and promotes the transcription of target genes involved in inflammation, cell survival, and other cancer-related processes. In cancer, aberrant activation of the NF-kB pathway is common. It can be triggered by various factors, including chronic inflammation, DNA damage, oncogenes, and tumour suppressor gene mutations. The persistent activation of NF-kB contributes to tumour growth and progression through several mechanisms: 1) NF-kB promotes cell survival and inhibits apoptosis by upregulating anti-apoptotic genes such as Bcl-2 and inhibitors of apoptosis proteins (IAPs). This prevents cancer cells from undergoing apoptosis; 2) NF-kB stimulates the expression of genes involved in inflammation and immune responses, creating a pro-inflammatory microenvironment that supports tumour growth and progression. Inflammation can induce the production of growth factors, cytokines, and chemokines that further promote angiogenesis, tissue remodelling, and cancer cell invasion; 3) NF-kB enhances the expression of genes involved in cell cycle progression and proliferation, contributing to uncontrolled cell growth in cancer cells. It can upregulate cyclins, cyclin-dependent kinases (CDKs), and growth-promoting factors, facilitating cell cycle progression and tumour cell proliferation; 4) NF-kB has also been implicated in promoting tumour angiogenesis. It induces the expression of pro-angiogenic factors such as VEGF and promotes endothelial cell survival and migration; 5) NF-kB also plays a role in cancer metastasis by regulating the expression of genes involved in epithelial-to-mesenchymal transition (EMT), a process where cancer cells acquire invasive and migratory properties. Overall, the dysregulation of NF-kB signaling contributes significantly to cancer development and progression by promoting cell survival, inflammation, proliferation, angiogenesis, and metastasis. We offer a large product range of research reagents for studying the NFkB pathway, including NF-kB p65 antibodies, Bcl10 antibodies, c-Rel antibodies, IKB alpha antibodies, and NF-kB p65 ELISA Kits. Explore our full NFkB pathway product range below and discover more, for less.