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The primary research interest of the Iron Biology Group is to understand the role of iron metabolism in complex diseases such as cancer and diabetes to identify biomarkers and pathways that can be of diagnostic, prognostic, and therapeutic value. Evidence suggests that estrogen (E2; 17-β estradiol) can manipulate iron metabolism through its ability to upregulate/downregulate the synthesis of the peptide hormone hepcidin. Which then negatively regulates the expression of the intracellular iron effluxing protein ferroportin (FPN). Increased hepcidin synthesis induces its internalization and degradation, and decreased hepcidin synthesis maintains its integrity as a plasma membrane-bound protein. Interestingly, recent studies have suggested that decreased levels of E2 could be a contributing factor to HCC development in males [Andrologia. 2016;48(9):948]. Also, ovariectomized female mice developed more frequent liver tumors than male mice, suggesting that E2 has a significant role in preventing HCC development [J Cell Biochem. 2018;119(10):8659].

Therefore, E2 may contribute to the regulation/dysregulation of intracellular as well as system iron homeostasis. The main focus of the ‘Iron Biology research group’ is to understand the molecular basis of this effect of E2and to evaluate its bearing on the onset/progression of diseases such as cancer, diabetes mellitus, and autoimmunity, among others. Collectively, this speaks of an E2-iron axis involved in various aspects of human physiology and pathophysiology. A better understanding of the molecular interactions underlying this E2-iron axis has the potential to lead to novel therapeutic approaches.