AIM: To investigate whether the iron stores regulator hepcidin is implicated in colon cancer-associated anaemia and whether it might have a role in colorectal carcinogenesis. METHODS: Mass spectrometry (MALDI-TOF MS and SELDI-TOF MS) was employed to measure hepcidin in urine collected from 56 patients with colorectal cancer. Quantitative Real Time RT-PCR was utilised to determine hepcidin mRNA expression in colorectal cancer tissue. Hepcidin cellular localisation was determined using immunohistochemistry. RESULTS: We demonstrate that whilst urinary hepcidin expression was not correlated with anaemia it was positively associated with increasing T-stage of colorectal cancer (P<0.05). Furthermore, we report that hepcidin mRNA is expressed in 34% of colorectal cancer tissue specimens and was correlated with ferroportin repression. This was supported by hepcidin immunoreactivity in colorectal cancer tissue. CONCLUSION: We demonstrate that systemic hepcidin expression is unlikely to be the cause of the systemic anaemia associated with colorectal cancer. However, we demonstrate for the first time that hepcidin is expressed by colorectal cancer tissue and that this may represent a novel oncogenic signalling mechanism.
AIM: To investigate whether the iron stores regulator hepcidin is implicated in colon cancer-associated anaemia and whether it might have a role in colorectal carcinogenesis. METHODS: Mass spectrometry (MALDI-TOF MS and SELDI-TOF MS) was employed to measure hepcidin in urine collected from 56 patients with colorectal cancer. Quantitative Real Time RT-PCR was utilised to determine hepcidin mRNA expression in colorectal cancer tissue. Hepcidin cellular localisation was determined using immunohistochemistry. RESULTS: We demonstrate that whilst urinary hepcidin expression was not correlated with anaemia it was positively associated with increasing T-stage of colorectal cancer (P<0.05). Furthermore, we report that hepcidin mRNA is expressed in 34% of colorectal cancer tissue specimens and was correlated with ferroportin repression. This was supported by hepcidin immunoreactivity in colorectal cancer tissue. CONCLUSION: We demonstrate that systemic hepcidin expression is unlikely to be the cause of the systemic anaemia associated with colorectal cancer. However, we demonstrate for the first time that hepcidin is expressed by colorectal cancer tissue and that this may represent a novel oncogenic signalling mechanism.
Authors: Erwin Kemna; Harold Tjalsma; Coby Laarakkers; Elizabeta Nemeth; Hans Willems; Dorine Swinkels Journal: Blood Date: 2005-07-19 Impact factor: 22.113
Authors: C Becker; M C Fantini; S Wirtz; A Nikolaev; H A Lehr; P R Galle; S Rose-John; M F Neurath Journal: Cell Cycle Date: 2005-02-03 Impact factor: 4.534
Authors: J D Hardcastle; J O Chamberlain; M H Robinson; S M Moss; S S Amar; T W Balfour; P D James; C M Mangham Journal: Lancet Date: 1996-11-30 Impact factor: 79.321
Authors: Naveen Sharma; Abas H Laftah; Matthew J Brookes; Brian Cooper; Tariq Iqbal; Chris Tselepis Journal: Biochem J Date: 2005-09-01 Impact factor: 3.857
Authors: D G Ward; N Suggett; Y Cheng; W Wei; H Johnson; L J Billingham; T Ismail; M J O Wakelam; P J Johnson; A Martin Journal: Br J Cancer Date: 2006-06-06 Impact factor: 7.640
Authors: Rachel M Ostroff; William L Bigbee; Wilbur Franklin; Larry Gold; Mike Mehan; York E Miller; Harvey I Pass; William N Rom; Jill M Siegfried; Alex Stewart; Jeffrey J Walker; Joel L Weissfeld; Stephen Williams; Dom Zichi; Edward N Brody Journal: PLoS One Date: 2010-12-07 Impact factor: 3.240