Abstract
An increasing amount of research has recently strengthened the case for the existence of iron dysmetabolism in prostate cancer. It is characterized with a wide array of differential expression of iron-related proteins compared to normal cells. These proteins control iron entry, cellular iron distribution but also iron exit from prostate cells. Iron dysmetabolism is not an exclusive feature of prostate cancer cells, but it is observed in other cells of the tumor microenvironment. Disrupting the machinery that secures iron for prostate cancer cells can retard tumor growth and its invasive potential. This review unveils the current understanding of the ways that prostate cancer cells secure iron in the tumor milieu and how can we exploit this knowledge for therapeutic purposes.
Highlights
Cancer cells are known for their voracious appetites for different metabolites and nutrients in order to satisfy their metabolic needs [1]
Iron dysregulation observed in experimental models with senescent prostate epithelial cells is intriguing and strikingly similar to prostate cancer (PCa) cells; it is characterized with TFR1, IRP2, ferritin upregulation, while FPN though upregulated, is mostly localized intracellularly, which means that it cannot participate in iron export [81]
The main changes include the overexpression of iron import proteins (TFR1), intracellular regulators of iron import (IRP2), proton pumps that cause intracellular iron release, and ferrireductases such as STAMP2
Summary
Edited by: Justin Lathia, Cleveland Clinic Lerner College of Medicine, United States. Reviewed by: Daniel Edward Frigo, University of Texas MD Anderson Cancer Center, United States. Specialty section: This article was submitted to Cancer Molecular Targets and Therapeutics, a section of the journal
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