Iron Metabolism and Cancer

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 3537

Special Issue Editors


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Guest Editor
Institute of Biotechnology of the Czech Academy of Sciences, BIOCEV Research Center, Vestec, Czech Republic
Interests: iron metabolism; cancer; cancer resistance; ABC transporters; apoptosis induction; mitochondria; cancer stem-like cells
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Institute of Biotechnology of the Czech Academy of Sciences, BIOCEV Research Center, Vestec, Czech Republic
Interests: iron metabolism; cancer; cancer resistance; apoptosis induction; mitochondria; mitophagy; mitochondrial targeting

Special Issue Information

Dear Colleagues,

Iron is an essential trace element that is required as a cofactor for many proteins including enzymes involved in mitochondrial respiration, cellular metabolism, and DNA replication. Iron also plays roles in the immune system and in the regulation of epigenetic modifications and gene transcription. It is thus not surprising that highly metabolically active and rapidly proliferating cells, including tumor cells, are dependent on iron.

I am pleased to announce a Special Issue of Metabolites entitled “Iron Metabolism and Cancer”, which aims to present the latest research on iron metabolism and the various functions of this essential trace metal element in relation to cancer initiation, progression, and metastasis. Submissions dealing with signaling, metabolic, and regulatory functions of iron in the context of tumor initiation, progression, metastasis, resistance, or treatment are welcome.

Dr. Jaroslav Truksa
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

iron uptake, storage, and export in cancer cells; iron sulfur clusters in cancer; heme iron and cancer; iron and hypoxia in cancer; iron and cellular metabolism in cancer iron metabolism and tumor initiation, progression and metastasis; iron metabolism and cancer resistance; iron metabolism and cancer diagnosis and treatment; iron and signaling pathways in cancer; iron and ROS in cancer; iron and epigenetic modifications in cancer; iron addiction in cancer; iron overload and cancer risk

 

Published Papers (1 paper)

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Research

19 pages, 4459 KiB  
Article
Iron-Bound Lipocalin-2 from Tumor-Associated Macrophages Drives Breast Cancer Progression Independent of Ferroportin
by Christina Mertens, Matthias Schnetz, Claudia Rehwald, Stephan Grein, Eiman Elwakeel, Andreas Weigert, Bernhard Brüne and Michaela Jung
Metabolites 2021, 11(3), 180; https://doi.org/10.3390/metabo11030180 - 19 Mar 2021
Cited by 15 | Viewed by 2978
Abstract
Macrophages supply iron to the breast tumor microenvironment by enforced secretion of lipocalin-2 (Lcn-2)-bound iron as well as the increased expression of the iron exporter ferroportin (FPN). We aimed at identifying the contribution of each pathway in supplying iron for the growing tumor, [...] Read more.
Macrophages supply iron to the breast tumor microenvironment by enforced secretion of lipocalin-2 (Lcn-2)-bound iron as well as the increased expression of the iron exporter ferroportin (FPN). We aimed at identifying the contribution of each pathway in supplying iron for the growing tumor, thereby fostering tumor progression. Analyzing the expression profiles of Lcn-2 and FPN using the spontaneous polyoma-middle-T oncogene (PyMT) breast cancer model as well as mining publicly available TCGA (The Cancer Genome Atlas) and GEO Series(GSE) datasets from the Gene Expression Omnibus database (GEO), we found no association between tumor parameters and Lcn-2 or FPN. However, stromal/macrophage-expression of Lcn-2 correlated with tumor onset, lung metastases, and recurrence, whereas FPN did not. While the total iron amount in wildtype and Lcn-2−/− PyMT tumors showed no difference, we observed that tumor-associated macrophages from Lcn-2−/− compared to wildtype tumors stored more iron. In contrast, Lcn-2−/− tumor cells accumulated less iron than their wildtype counterparts, translating into a low migratory and proliferative capacity of Lcn-2−/− tumor cells in a 3D tumor spheroid model in vitro. Our data suggest a pivotal role of Lcn-2 in tumor iron-management, affecting tumor growth. This study underscores the role of iron for tumor progression and the need for a better understanding of iron-targeted therapy approaches. Full article
(This article belongs to the Special Issue Iron Metabolism and Cancer)
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