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Macrophage functionality in obesity favors cancer progression.

Obesity has a profound influence on the progression of many diseases. It induces multi-factorial effects such as dyslipidemia, insulin resistance, diabetes, arterial hypertension, and increased incidences of cancers. Multiple mechanisms link obesity with cancer initiation and progression; however, the least studied is the role of macrophages. Nutritional overload causes adipose tissue expansion in obesity and alters the balance between pro- and anti-inflammatory macrophages, which becomes a primary cause of inflammation. The chronic low-grade inflammation driven by macrophages is also an important characteristic of cancer. Adipose tissue secretes various adipokines, namely adiponectin, leptin, IL-6, TNF-α, etc., which influence macrophage behavior and tumor progression. Furthermore, other metabolic effects of obesity, such as hyperlipidemia, hyperglycemia, and hypercholesterolemia, can also regulate macrophage functionality towards tumor cells. This review summarizes events and mechanisms by which obesity influences macrophage-tumor cell interactions. The role of macrophages in anti-cancer therapies under obese conditions, as well as the effect of macrophages on T cells to regulate tumor progression, are also highlighted.