Iron and colorectal cancer: evidence from in vitro and animal studies

Abstract

Iron is a vital trace element essential for mammalian life. It is involved in numerous biological and cellular processes such as oxygen transport, oxidative phosphorylation, and DNA synthesis, as well as cell cycle progression and growth. Normal and neoplastic cells have similar qualitative requirements for iron. In addition, research shows that iron promotes cancer cell growth. An adequate balance of iron is, therefore, critical for health. In states of iron deficiency, anemia can develop, whereas iron excess increases oxidative stress in body tissues, leading to lipid, protein, and DNA damage via the Fenton reaction, which results in the synthesis of hydroxyl radicals and other oxidants. It is thought that some of these processes are implicated in the pathogenesis of colorectal cancer. This review provides the clinician with an up-to-date summary of the recent advances in this field using established in vitro and animal models.

Keywords: Wnt signaling; colorectal cancer; heme; iron; oxidative stress.