The Role of Cytokines, Chemokines and NFkB in Inflammation and Cancer

Abstract

Previous researches have suggested that chronic inflammation plays a critical role in cancer pathogenesis as it has been assessed that underlying infections and inflammatory responses have been associated with 25% of all cancer cases, whereas the inflammatory microenvironment is an essential component of all tumors. Moreover, some of the molecular mechanisms that link the mentioned association have been clarified. Cancer pathogenesis has been associated with physical mutations and environmental factors, whereas a limited rate has been associated with germline mutations. The special role of environmental factors in cancer pathogenesis has been associated with diverse types of chronic inflammation. It has been recorded that 30% of cancer cases can be attributed to smoking and inhaled pollutants, such as asbestos and carbon dioxide silicon, 20% are associated with chronic infections, and 35% are related to nutrition factors. Common bacterial and viral infections increase the risk of cancer development, however smoking acts as a promoter due to its ability to cause chronic inflammation. Similarly, advanced age and cellular senescence has been recorded to have the same role, as cancer pathogenesis promoters, because act through inflammatory mechanisms. Cellular senescence and damaged DNA accumulation are able to enhance chronic inflammation which promotes tumorigenesis. Inflammation-induced cancer contributes to tumor development through different pathways, such as epigenetic alterations and subsequent inappropriate gene expression, gene instability induction, increased proliferation and resistance to apoptosis of the initial cells, immuno-suppression, induction of tumor angiogenesis, tissue remodeling, and eventually development of metastasis.