Chronic Inflammatory Mediators in Tumor Microenvironment Induced Tumor Progression

Shrihari T.G

Abstract

Inflammation is the body’s defensive action against noxious stimuli such as physical or chemical or thermal or infectious agents by inflammatory mediators released from the innate and adaptive immune cells. If the  inflammation is aggrevated, chronic, nonresolving, and smoldering  inflammation in dysregulated  immune cells  results in releasing various  inflammatory mediators  such as chemokines, cytokines, growth factors, and proteolytic enzymes produced from chronic inflammatory cells such as neutrophils , macrophages, mast cells, basophils, T cells, and B cells in the tumor microenvironment. IL-1β,TNF-α, and COX-2 pro-inflammatory mediators released from chronic inflammatory cells  activate key transcription factors including  NF-KB, STAT3, HIF-1α and AP-1 which work together and cause cell proliferation by activation of cyclin D cell cycle regulatory protein, angiogenesis by IL-8,VEGF inflammatory mediators, immuno-suppression by IL-10,TGF-β,  cell survival by activation of BCL-2,BCL-XL anti-apoptotic proteins, genomic instability by release of ROS,RNS free radicals, invasion and metastasis by release of proteolytic enzymes such as (UPA, Mmp 2,9). This article described the role of chronic inflammatory innate and adaptive immune cells and their mediators in tumor microenvironment involved in tumor progression.



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