Regulation of cellular iron metabolism and its implications in lung cancer progression.

Abstract

Iron is essential for life and is involved in numerous metabolic processes including cell growth and proliferation. However, excess iron in the body raises the risk of developing cancer due to its capacity to engage in redox cycling and free radical production. Therefore, iron can contribute to both carcinogenesis and tumor growth. Both epidemiologic and laboratory studies have demonstrated that the effects of iron overload are associated with the tumorigenesis of lung cancer and growth of lung cancer cells. In particular, the discovery of hepcidin and several iron transporters in the past decade may warrant reconsideration of the role of iron in carcinogenesis and tumor cell proliferation in lung cancer. Pathways of iron uptake, storage, efflux, and regulation are all disturbed in cancer, suggesting that reprogramming of iron metabolism is a critical aspect of tumor cell survival. Although these pathways in lung cancer have been identified and extensively studied, many issues on the metabolic processes of iron in lung cancer cells have not been addressed. Targeting metabolic pathways of iron may provide new tools for lung cancer prognosis and therapy.