The Role of Inflammation and Changes of Adipose Tissue-Resident Immune Cells in Increasing the Risk of Cancer: A Narrative Review

The incidence of obesity, as a major health problem, has increased significantly over the past decades. This condition is associated with an increased risk of cancers, type 2 diabetes, and cardiovascular diseases. The current study aimed to investigate the effects of inflammation and changes of adipose tissue-resident immune cells on increasing the risk of cancer in obese individuals. In obesity, an increase in white adipose tissue changes the phenotype of tissue-resident macrophages to M1, resulting in chronic inflammation. This, in turn, increases the number of immune suppressor cells (e.g., regulatory T cells and myeloid-derived suppressor cells in white adipose tissue), but inhibits the anti-tumor activity of natural killer cells. Besides, hormonal and metabolic changes caused by obesity increase the risk of cancer. The elevated levels of hormones, such as insulin and leptin, activate the mitogenic Ras/MAPK pathway, and transduce inhibitory signals of apoptotic death in cancer cells. Also, the white adipose tissue acts as an energy source for cancer cells and promotes tumor growth and metastasis by producing pro-inflammatory cytokines, adipokines, and proangiogenic factors. Overall, obesity, by increasing the white fat mass, prepares a suitable microenvironment for triggering tumor formation and inhibiting anti-tumor pathways, which increase the risk of cancers.