Читать книгу Biomolecular Engineering Solutions for Renewable Specialty Chemicals - Группа авторов - Страница 74

NF‐κB is one of the transcription factors, which is abnormally regulated in disease like cancer. Activation of NF‐κB has been documented in various cancers, including liver, colon, pancreas, breast, prostrate, ovarian, leukemia, and lymphoma cancers and others also. DNA damaging also activates NF‐κB, which in turn activates and regulates a number of NF‐κB‐influenced target genes, including inducible nitric oxide synthase, and COX‐2. Furthermore, binding of TNF‐α to TNFR leads to homotrimerization of receptors and adaptor proteins resulting in cell proliferation and survival by increasing the expression of NF‐κB and activator protein 1 target genes, including vascular cell adhesion molecule‐1 (VCAM‐1). NF‐κB activation triggers the activation of chemokines and its related receptors, including C‐X‐C chemokine receptor 4 (CXCR4) and CCR7, which play crucial role in cancer cells’ migration to target organs. These genes play major roles in antiapoptosis process. Vanilla‐containing foods have the potential of therapeutic efficacy against cancer by inhibiting NF‐κB pathway activation in cancer cells. In lipopolysaccharide‐induced MCF‐7 cells, Z138 cells, T24, and THP1 cells, vanilla inhibits proliferation, adhesion, migration, and invasion by regulating the NF‐κB pathway. In the NF‐κB pathway, vanilla also reported to inhibit the expression of inflammatory factors TNF‐α and IL‐6 and abnormal NF‐κB activation through inhibition of phospho‐IκBα, p65 and upregulation of miR16 (Lirdprapamongkol et al., 2010). Vanilla also showed the inhibition of the NF‐κB nuclear translocation leading to the inhibition of mRNA expression and COX‐2, VCAM, and ICAM proteins.