title: Hepcidin expression in the liver of mice with implanted tumour reacts to iron deficiency, inflammation and erythropoietin administration.
abstract: Cancer is known to be an important cause           of anaemia due to several factors including iron deficiency           and inflammation. Hepcidin, a key regulator           of iron metabolism, is up-regulated by iron and inflammatory           stimuli such as interleukin 6, and decreased           by iron deficiency, enhanced erythropoiesis           and hypoxia. It is supposed to play a crucial role in           changes of iron metabolism in anaemia of chronic           disease, which is characterized by sequestering iron           in macrophages and decreasing its availability for           red blood cell production. To study the effect of tumour           growth on hepcidin expression, we implanted           human melanoma cells into mice and studied the           changes of the amount of liver hepcidin mRNA by           real-time PCR. We observed development of anaemia,           which correlated with the size of the tumour.           Hepcidin expression significantly decreased with the           anaemia development, but in late stages we observed           an increase of its expression together with an increase           of mRNA for interleukin 6. However, the increase of           hepcidin expression could be inhibited by exogenous           erythropoietin administration. In our model of tumour           growth, hepcidin expression reflected anaemia           development and iron deficiency, erythropoietin administration           and inflammation, and we suppose that           it could therefore serve as a useful marker of these           clinical situations common in cancer patients and           play a role in the pathogenesis of cancer-associated           anaemia.
authors.affiliation: Institute of Pathophysiology and Centre for Experimental Haematology, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic. mvoku@lfl.cuni.cz
authors.forename: M
authors.initials: M
authors.lastname: Vokurka
authors.forename: J
authors.initials: J
authors.lastname: Krijt
authors.forename: J
authors.initials: J
authors.lastname: Vávrová
authors.forename: E
authors.initials: E
authors.lastname: Nečas
mesh_terms: D000740:Anemia / Q000150:complications / Q000473:pathology; D000818:Animals; D023181:Antimicrobial Cationic Peptides / Q000235:genetics / Q000378:metabolism*; D049109:Cell Proliferation / Q000187:drug effects; D004921:Erythropoietin / Q000008:administration & dosage* / Q000494:pharmacology; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D064451:Hepcidins; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000473:pathology*; D007279:Injections, Subcutaneous; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D000090463:Iron Deficiencies; D008099:Liver / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008545:Melanoma / Q000150:complications / Q000235:genetics / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D023041:Xenograft Model Antitumor Assays
chemical_list: D023181:Antimicrobial Cationic Peptides; C578702:HAMP protein, human; C579599:Hamp protein, mouse; D064451:Hepcidins; D015850:Interleukin-6; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D004921:Erythropoietin