Colorectal cancer (CRC) is the third most common cause of
cancer-related deaths in industrialized countries. Understanding the mechanisms of growth and progression of CRC is essential to improve treatment.
Iron is an essential nutrient for cell growth.
Iron overload caused by hereditary mutations or excess
dietary iron uptake has been identified as a risk factor for CRC. Intestinal
iron is tightly controlled by
iron transporters that are responsible for
iron uptake, distribution, and export. Dysregulation of intestinal
iron transporters are observed in CRC and lead to
iron accumulation in
tumors. Intratumoral
iron results in oxidative stress, lipid peroxidation,
protein modification and DNA damage with consequent promotion of oncogene activation. In addition, excess
iron in intestinal
tumors may lead to increase in
tumor-elicited
inflammation and
tumor growth. Limiting intratumoral
iron through specifically chelating excess intestinal
iron or modulating activities of
iron transporter may be an attractive therapeutic target for CRC.