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Influence of iron on the gut microbiota in colorectal cancer
Phipps, Oliver Al-Hassi, Hafid Omar Quraishi, Mohammed N Kumar, Aditi
Phipps, Oliver
Al-Hassi, Hafid Omar
Quraishi, Mohammed N
Kumar, Aditi
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2020-08-20
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Abstract
Perturbations of the colonic microbiota can contribute to the initiation and progression of colorectal cancer, leading to an increase in pathogenic bacteria at the expense of protective bacteria. This can contribute to disease through increasing carcinogenic metabolite/toxin production, inducing inflammation, and activating oncogenic signaling. To limit disease progression, external factors that may influence the colonic microbiota need to be considered in patients with colorectal cancer. One major factor that can influence the colonic microbiota is iron. Iron is an essential micronutrient that is required by both prokaryotes and eukaryotes for cellular function. Most pathogenic bacteria have heightened iron acquisition mechanisms and therefore tend to outcompete protective bacteria for free iron. Colorectal cancer patients often present with anemia due to iron deficiency, and thus they require iron therapy. Depending upon the route of administration, iron therapy has the potential to contribute to a procarciongenic microbiota. Orally administered iron is the common treatment for anemia in these patients but can lead to an increased gut iron concentration. This suggests the need to reassess the route of iron therapy in these patients. Currently, this has only been assessed in murine studies, with human trials being necessary to unravel the potential microbial outcomes of iron therapy.
Citation
Phipps, O.; Al-Hassi, H.O., Quraishi, M.N., Kumar, A. and Brookes, M. J. (2020) Influence of iron on the gut microbiota in colorectal cancer. Nutrients, 12, 2512.
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Journal article
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en
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© 2020 The Authors. Published by MDPI. This is an open access article available under a Creative Commons licence.
The published version can be accessed at the following link on the publisher’s website: https://doi.org/10.3390/nu12092512
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2072-6643
EISSN
2072-6643