Role of activation-induced cytidine deaminase in inflammation-associated cancer development.

摘要: Human cancer is a genetic disease resulting from the stepwise accumulation of alterations in various tumor-related genes. Normal mutation rates, however, cannot account for abundant changes accumulated tumor cells, suggesting that certain molecular mechanisms underlie such large number alterations. Activation-induced cytidine deaminase (AID), nucleotide-editing enzyme triggers DNA and double-strand breaks immunoglobulin gene, has been identified activated B lymphocytes. Recent studies revealed AID-mediated genotoxic effects target not only genes but also variety other both lymphocytes non-lymphoid cells. Consistent with finding several transcription factors including nuclear factor-κB (NF-κB) mediate AID expression proinflammatory cytokine stimulation types gastrointestinal epithelial as gastric, colonic, hepatic, biliary epithelium, induces aberrant through NF-κB signaling pathway. In vivo constitutive promotes tumorigenic pathway by enhancing susceptibility to mutagenesis organs. The activity genome mutator provides new avenue aimed at understanding during carcinogenesis.