The Role of the Mediators of Inflammation in Cancer Development

Abstract

Epigenetic disorders such as point mutations in cellular tumor suppressor genes, DNA methylation and post-translational modifications are needed to transformation of normal cells into cancer cells. These events result in alterations in critical pathways responsible for maintaining the normal cellular homeostasis, triggering to an inflammatory response which can lead the development of cancer. The inflammatory response is a universal defense mechanism activated in response to an injury tissue, of any nature, that involves both innate and adaptive immune responses, through the collective action of a variety of soluble mediators. Many inflammatory signaling pathways are activated in several types of cancer, linking chronic inflammation to tumorigenesis process. Thus, Inflammatory responses play decisive roles at different stages of tumor development, including initiation, promotion, growth, invasion, and metastasis, affecting also the immune surveillance. Immune cells that infiltrate tumors engage in an extensive and dynamic crosstalk with cancer cells, and some of the molecular events that mediate this dialog have been revealed. A range of inflammation mediators, including cytokines, chemokines, free radicals, prostaglandins, growth and transcription factors, microRNAs, and enzymes as, cyclooxygenase and matrix metalloproteinase, collectively acts to create a favorable microenvironment for the development of tumors. In this review are presented the main mediators of the inflammatory response and discussed the likely mechanisms through which, they interact with each other to create a condition favorable to development of cancer.

Dietary inflammatory index and inflammatory biomarkers in adolescents from LabMed physical activity study

“…Low-grade inflammation correlates with a set of chronic conditions [1,2] such as obesity [3], diabetes [3,4], cardiovascular diseases [5,6] and cancer [7,8]. This association has also been found in youth for obesity [9][10][11], central obesity [12,13], metabolic syndrome [14,15], atherosclerosis [16], and several other cardiovascular risk factors [10,13].…”

Down-regulated and Commonly mutated ALPK1 in Lung and Colorectal Cancers

“…Relatedly, epidemiological studies have suggested that chronic inflammation may tend to initiate cancer through DNA damage or mutations that are affected by reactive oxygen species and some nitrogen derivatives2. According to clinical research, patients with an inflammatory bowel disease, such as Crohn’s disease or ulcerative colitis, have a high risk of suffering from colorectal cancer3.…”

Nanoparticulate immunotherapy for cancer

“…On the other hand, a range of inflammation mediators [cytokines, chemokines, free radicals, prostaglandins, transcription factors, microRNAs, and enzymes such as, arginase (ARG1), indoleamine 2,3-dioxygenase (IDO), cyclooxygenase and matrix metalloproteinase (MMP), nitric oxide synthase (NOS2)] are released by or reside in cancer cells and immune cells, collectively act to create a favorable microenvironment for the development of tumors. Transforming growth factor β (TGF-β) and IL-10 are the major immune suppressive cytokines secreted by tumor cells, MDSC, and TAMs while several proinflammatory cytokines (IL-1, IL-6, TNF-α) that mediate chronic inflammation in the tumor, significantly contribute to tumorigenesis and progression [27].…”