Overexpression of insulin-like growth factor-I receptor as a pertinent biomarker for hepatocytes malignant transformation

AIM: To investigate the dynamic features of insulin-like growth factor-I receptor (IGF-I R) expression in rat hepatocarcinogenesis, and the relationship between IGF-I R and hepatocytes malignant transformation at mRNA or protein level. METHODS: Hepatoma models were made by inducing with 2-fluorenylacetamide (2-FAA) on male Sprague-Dawley rats. Morphological changes of hepatocytes were observed by pathological Hematoxylin and eosin staining, the dynamic expressions of liver and serum IGF-I R were quantitatively analyzed by an enzymelinked immunosorbent assay. The distribution of hepatic IGF-I R was located by immunohistochemistry. The fragments of IGF-I R gene were amplified by reverse transcription-polymerase chain reaction, and confirmed by sequencing. RESULTS: Rat hepatocytes after induced by 2-FAA were changed dynamically from granule-like degeneration, precancerous to hepatoma formation with the progressing increasing of hepatic mRNA or IGF-I R expression. The incidences of liver IGF-I R, IGF-I R mRNA, specific IGF-I R concentration (ng/mg wet liver), and serum IGF-I R level (ng/mL) were 0.0%, 0.0%, 0.63 +/- 0.17, and 1.33 +/- 0.47 in the control; 50.0%, 61.1%, 0.65 +/- 0.2, and 1.51 +/- 0.46 in the degeneration; 88.9%, 100%, 0.66 +/- 0.14, and 1.92 +/- 0.29 in the precancerosis; and 100%, 100%, 0.96 +/- 0.09, and 2.43 +/- 0.57 in the cancerous group, respectively. IGF. R expression in the cancerous group was significantly higher (P < 0.01) than that in any of other groups at mRNA or protein level. The closely positive IGF-I R relationship was found between livers and sera (r = 0.91, t = 14.222, P < 0.01), respectively. CONCLUSION: IGF-I R expression may participate in rat hepatocarcinogenesis and its abnormality should be an early marker for hepatocytes malignant transformation. (C) 2013 Baishideng. All rights reserved.