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. Author manuscript; available in PMC: 2017 Mar 1.
Published in final edited form as: Trends Biochem Sci. 2015 Dec 23;41(3):274–286. doi: 10.1016/j.tibs.2015.11.012

Figure 3. The Ferroportin–Hepcidin Axis Is Altered in Cancers.

Figure 3

Normal breast and prostate cells (right) contain relatively low intracellular iron as a result of high ferroportin, low hepcidin, and low TfR1 expression. By contrast, breast and prostate cancer cells (left) often have elevated TfR1 as well as low ferroportin expression because of hypermethylation of the ferroportin promoter which inhibits Fpn transcription factors (Nrf2, MZF1). In addition, post-translational repression of Fpn by tumor- and liver-derived hepcidin further blocks iron efflux. Consequently, these cancer cells can aberrantly accumulate intracellular iron, leading to increased cell proliferation and an aggressive cancer phenotype.