Figure 2.
The activation of the NF-κB in breast cancer microenvironment. NF-κB interacts with and activates various signaling pathways, which eventually result in BC progression. TLRs, Toll-like receptors; TNFRs, TNF-α receptors; TCR, T cell receptor; BCR, B cell receptor; LTβR, lymphotoxin β receptor; BAFFR, the BAFF receptor; RANK, receptor activator of nuclear factor-kappa beta; BC cell, breast cancer cell; PI3K, phosphoinositide 3-kinase; ERK, extracellular signal-related kinase; HER2, human epidermal growth factor receptor 2; ER, estrogen receptor; NF-κB, nuclear factor-kappa beta of activated B cell; EGFR, epidermal growth factor receptor; mbER, membrane-bound ER; SRC3, steroid coactivator 3; MMP-9, matrix metalloproteinase-9; TGF-β, transforming growth factor-β; BIRC-3, baculoviral IAP repeat-containing 3; cIAP-2, cellular inhibitor of apoptosis protein; XPB-1, X-box binding protein-1; Bcl-2, B cell lymphoma-2; IL-6, interleukin 6; IL-17, interleukin 17; HIF-1α, hypoxia-inducible factor 1 alpha; VEGF, vascular endothelial growth factor; IL-6R, interleukin 6 receptor; EMT; epithelial-to-mesenchymal transition; PD-L1, programmed cell death receptor 1 ligand; IFN-γ, interferon gamma; STAT, signal transducer and activator of transcription. Note: For more information, please see the text.
