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Expression of hepcidin mRNA is uniformly suppressed in hepatocellular carcinoma

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Abstract Background The present study evaluated the expression of hepcidin mRNA in hepatocellular carcinoma (HCC). Methods Samples of cancerous and non-cancerous liver tissue were taken from 40 patients with HCC who underwent hepatectomy. Expression of hepcidin mRNA was evaluated by real-time PCR, and compared in tumors differing in their degree of differentiation, number of tumors, and vessel invasion. Correlations between hepcidin expression and the interval until HCC recurrence, and the serum concentration of hepcidin were evaluated, together with the expression of mRNAs for other iron metabolism molecules, ferroportin and transferrin receptor 2 (Trf2). Results Hepcidin mRNA expression in non-cancerous and cancerous tissues was 1891.8 (32.3–23187.4) and 53.4 (1.9–3185.8), respectively (P < 0.0001). There were no significant differences in hepcidin expression among tumors differing in their degree of differentiation, number of tumors, or vessel invasion. There was no significant correlation between hepcidin expression and the interval until HCC recurrence. The serum concentration of hepcidin-25 was not correlated with hepcidin-mRNA expression. Finally, there were no significant differences in the expression of mRNA for ferroportin and Trf2 between cancerous and non-cancerous tissues. Conclusion Expression of hepcidin mRNA is strikingly suppressed in cancerous, but not in non-cancerous tissues, in patients with HCC, irrespective of ferroportin or Trf2 expression. Uniform suppression of hepcidin may be linked to the development of HCC.
Title: Expression of hepcidin mRNA is uniformly suppressed in hepatocellular carcinoma
Description:
Abstract Background The present study evaluated the expression of hepcidin mRNA in hepatocellular carcinoma (HCC).
Methods Samples of cancerous and non-cancerous liver tissue were taken from 40 patients with HCC who underwent hepatectomy.
Expression of hepcidin mRNA was evaluated by real-time PCR, and compared in tumors differing in their degree of differentiation, number of tumors, and vessel invasion.
Correlations between hepcidin expression and the interval until HCC recurrence, and the serum concentration of hepcidin were evaluated, together with the expression of mRNAs for other iron metabolism molecules, ferroportin and transferrin receptor 2 (Trf2).
Results Hepcidin mRNA expression in non-cancerous and cancerous tissues was 1891.
8 (32.
3–23187.
4) and 53.
4 (1.
9–3185.
8), respectively (P < 0.
0001).
There were no significant differences in hepcidin expression among tumors differing in their degree of differentiation, number of tumors, or vessel invasion.
There was no significant correlation between hepcidin expression and the interval until HCC recurrence.
The serum concentration of hepcidin-25 was not correlated with hepcidin-mRNA expression.
Finally, there were no significant differences in the expression of mRNA for ferroportin and Trf2 between cancerous and non-cancerous tissues.
Conclusion Expression of hepcidin mRNA is strikingly suppressed in cancerous, but not in non-cancerous tissues, in patients with HCC, irrespective of ferroportin or Trf2 expression.
Uniform suppression of hepcidin may be linked to the development of HCC.

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