Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Feb 2;50(2):e436. doi: 10.1038/emm.2017.273

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2018 The Author(s)

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

PMC Copyright notice

Hepcidin regulation in cancer tissue. Hepcidin in cancer tissue is produced by local tumor cells and liver. Hepcidin overexpression in tumor tissue is related to different bone morphogenetic protein (BMP) molecules (such as BMP7) as well as to inflammatory stimuli, such as interleukin-6 (IL-6). Studies suggest the existence of new regulators of hepcidin in cancer tissue such as sclerostin domain-containing protein 1 (SOSTDC1) (which is downregulated in cancer through epigenetic silencing) and the Wnt pathway (which is upregulated in cancer). Increased hepcidin in the tumor milieu induces iron sequestration in tumor cells through its actions on ferroportin (FPN). Hepcidin increase is accompanied by tumor transferrin receptor 1 (TFR1) upregulation, which increases iron supply into tumor cells. Increased iron depots in tumor cells help them survive and proliferate.