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Expression of insulin‐like growth factor II mRNA in hepatocellular carcinoma
Author(s) -
NG IRENE OL,
LEE JOYCE MF,
SRIVASTAVA GOPESH,
NG MATTHEW
Publication year - 1998
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.1998.tb00630.x
Subject(s) - hepatocellular carcinoma , insulin like growth factor 2 , northern blot , promoter , gene expression , messenger rna , growth factor , cancer research , immunohistochemistry , insulin like growth factor , medicine , biology , gene , pathology , endocrinology , receptor , biochemistry
Insulin‐like growth factor II (IGF‐II) is a mitogenic polypeptide closely related to insulin. Its gene has complex regulation of transcription, resulting in multiple mRNA initiated by different promoters. To study its role in hepatocarcinogenesis, we examined the expression of IGF‐II mRNA in hepatocellular carcinomas (HCC) and correlated it with the pathological features of the tumours. Using northern blot analysis, transcription of the normal adult promoter was repressed in all but two of the 30 HCC. Instead, there was re‐expression of two foetal transcripts (6 and 5 kb) in 12 tumours. In contrast, most (93.3%) of the non‐tumorous livers showed expression of adult transcript only, and there were three livers demonstrating expression of foetal transcripts in addition to the adult one. There was a significant association of IGF‐II expression with direct tumour invasion into the adjacent liver parenchyma but foetal expression did not influence other parameters directly related to tumour invasiveness, including venous permeation, formation of tumour microsatellites and positive resection margin. Besides, IGF‐II expression was significantly more frequently seen in tumours from older patients. To conclude, repression of normal adult promoter and re‐expression of foetal promoters of IGF‐II are common events in HCC. The observation that foetal IGF‐II expression was significantly more frequent in older patients suggests that spontaneous foetal expression of IGF‐II late in life may promote the growth of tumours which have already arisen through other mechanisms, but foetal reexpression itself is not enough to contribute to tumour progression.