Inflammation is a primary response of the host to any infections and tissue damage, and it is characterized by a series of reactions. In general, it is accepted that inflammation is beneficial to the host, but it should be resolved in a timely manner. Persistent infection cumulatively causes successive inflammatory reactions, which dysregulates innate and/or adaptive immune functions and makes people susceptible to several diseases. Several shreds of evidence are suggesting that cancers originated due to failure in the host immunity and persistent inflammatory reactions. Amongst various signalling pathways, signalling mediated by NF- κB, COX-2, and JAK/STAT seems to play a major role in tumorigenesis. Several inflammatory markers are identified (Tumor Necrosis Factor-a (TNF-α, Interleukin-6 (IL-6), and C-Reactive Protein (CRP)), and regulated by several fold in response to infection and tissue damage vis a vis in proliferation, Epithelial- Mesenchymal Transition (EMT), invasion, and metastasis.
Chronic inflammation is known to elicit carcinogenesis and metastasis at distant sites either through direct interactions of inflammatory cells and cancer cells or indirect effects of inflammatory cells on other resident stromal cells. Chronic activation of the immune system by microbial infection is associated with tumors at numerous sites. In this review article, we are discussing how chronic inflammation is prone to developing disease and the role of inflammatory signalling markers in cancer development and progression and tumor microenvironment profile. We need to identify the novel inflammatory biomarkers which are significantly associated with chronic inflammation and cancer development; it might be helpful for the patients with a better therapeutic approach.Author(s): Santhoshi Rani Nanchari, Satti Vishnupriya, Vijayalakshmi Venkatesan