| First Author | Wu CG | Year | 1997 |
| Journal | Carcinogenesis | Volume | 18 |
| Issue | 1 | Pages | 47-52 |
| PubMed ID | 9054589 | Mgi Jnum | J:38604 |
| Mgi Id | MGI:85991 | Doi | 10.1093/carcin/18.1.47 |
| Citation | Wu CG, et al. (1997) Rat ferritin-H: cDNA cloning, differential expression and localization during hepatocarcinogenesis. Carcinogenesis 18(1):47-52 |
| abstractText | Elevated serum ferritin levels, especially of the H subunit, accompany many clinical malignancies. By using the subtraction-enhanced display technique, we have recently isolated several cDNA clones which are over-expressed in rat hepatocellular carcinoma induced by diethylnitrosamine. One 830-base-pair clone was 88% similar to human ferritin-H cDNA and encoded a 182 amino acid protein which is 97% homologous to human ferritin-H chain. Hepatic mRNA levels of ferritin-H were increased markedly at the early stage of diethylnitrosamine-induced hepatocarcinogenesis in the rat (6 weeks) and appeared more than 10-fold overexpressed as the tumour progressed. In contrast, hepatic ferritin-H mRNA remained constant during liver regeneration after a 70% partial hepatectomy. In situ hybridization showed that over-expression of ferritin-H was exclusively localized to preneoplastic foci, to tumour nodules and to tumour cells invading blood vessels. These findings suggest that ferritin-H is a highly conserved protein, its over-expression during tumour development is phenotypically correlated with tumour initiation and/or progression, and it is useful as an early marker for hepatocellular carcinoma. |
