Expression of stem cell factor receptor c-kit in human nontumoral and tumoral hepatic cells

Eur J Gastroenterol Hepatol. 2009 Oct;21(10):1206-11. doi: 10.1097/MEG.0b013e328317f4ef.

Abstract

Introduction: The aim of this study was to examine and compare the stem cell factor receptor c-kit expression in hepatocellular carcinoma (HCC) with the corresponding peritumoral tissue. To confirm the immunohistochemical results in the investigated HCC tissues, HCC cell lines were analyzed for c-kit expression.

Methods: Expression of c-kit (SCF receptor) has been evaluated in 72 HCC and in the corresponding surrounding nontumorous tissue. Additionally, immunohistochemical analysis reverse transcription-polymerase chain reaction was also used to examine the mRNA expression of c-kit protooncogene in tumor homogenates. Furthermore, three HCC cell lines (HUH-7, HepG2, and SK-Hep1) were used for gene-expression analysis of c-kit mRNA.

Results: C-kit expression was detected immunohistochemically in 70% of HCC with different degrees of intensity. Moreover, c-kit expression could also be found in about 90% of the corresponding peritumoral noncirrhotic as well as in cirrhotic liver tissues. C-kit mRNA was detectable in 83% of HCC and in 75% of the corresponding peritumoral noncirrhotic as well as in 100% of corresponding peritumoral cirrhotic samples. In addition, two of the three HCC cell lines (HUH-7 and SK-Hep1) showed a well detectable PCR-product for c-kit.

Conclusion: Hepatocytes express the c-kit receptor at different grade of intensity under normal and altered pathological conditions. The presence of c-kit on HCC cell lines supports the assumption that SCF might play a role in the regulation of proliferative activity of tumorous and nontumorous hepatic cells.

MeSH terms

  • Carcinoma, Hepatocellular / etiology
  • Carcinoma, Hepatocellular / metabolism*
  • Carcinoma, Hepatocellular / pathology
  • Gene Expression
  • Hepatocytes / metabolism*
  • Humans
  • Liver Cirrhosis / complications
  • Liver Cirrhosis / metabolism
  • Liver Neoplasms / etiology
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / pathology
  • Proto-Oncogene Proteins c-kit / genetics
  • Proto-Oncogene Proteins c-kit / metabolism*
  • RNA, Messenger / genetics
  • RNA, Neoplasm / genetics
  • Reverse Transcriptase Polymerase Chain Reaction / methods
  • Tumor Cells, Cultured

Substances

  • RNA, Messenger
  • RNA, Neoplasm
  • Proto-Oncogene Proteins c-kit