Unraveling the molecular mechanisms between inflammation and tumor angiogenesis

Inflammatory mediators in tumor microenvironment influence cancer occurrence, growth and metastasis through complex signaling networks. Excessive inflammation is closely associated with elevated cancer risk and mortality, in part through inflammation-induced angiogenesis. Mechanistically, multiple tumor-associated inflammatory cells increase the release and accumulation of various inflammatory products in cancerous sites. These products in turn activate tumor associated signaling cascades such as STAT3, NF-kappa B, PI3K/Akt and p38 MAPK, which mediate the recruitment of inflammatory cells and secretion of pro-inflammatory factors. More importantly, these events promote the secretion of various pro-angiogenesis factors from endothelial, tumor and inflammatory cells, which then drive malignancy in endothelial cells in a paracrine and/or autocrine manner. Its ultimate effect is to promote endothelial cell proliferation, migration, survival and tube formation, and to hence the formation of blood vessels in tumors. This review describes the signaling network that connects the interaction between inflammation and cancer, especially those involved in inflammation-induced angiogenesis. This will reveal potential targets for the design of anti-inflammatory treatments and drugs that inhibites tumor growth and angiogenesis.

Automated summary

Inflammatory mediators in the tumor microenvironment play a critical role in influencing cancer occurrence, growth, and metastasis. Excessive inflammation is closely associated with increased cancer risk and mortality, partly through inflammation-induced angiogenesis. The complex signaling networks involved in inflammation-induced angiogenesis provide potential targets for the design of anti-inflammatory treatments and drugs that inhibit tumor growth.