title: Peroxisome proliferator-activated receptor α (PPARα) mRNA expression in human hepatocellular carcinoma tissue and non-cancerous liver tissue.
abstract: BACKGROUND
  Peroxisome proliferator-activated receptor α (PPARα) regulates lipid metabolism in the liver. It is unclear, however, how this receptor changes in liver cancer tissue. On the other hand, mouse carcinogenicity studies showed that PPARα is necessary for the development of liver cancer induced by peroxisome proliferators, and the relationship between PPARα and the development of liver cancer have been the focus of considerable attention. There have been no reports, however, demonstrating that PPARα is involved in the development of human liver cancer.
  
  
  METHODS
  The subjects were 10 patients who underwent hepatectomy for hepatocellular carcinoma. We assessed the expression of PPARα mRNA in human hepatocellular carcinoma tissue and non-cancerous tissue, as well as the expression of target genes of PPARα, carnitine palmitoyltransferase 1A and cyclin D1 mRNAs. We also evaluated glyceraldehyde 3-phosphate dehydrogenase, a key enzyme in the glycolytic system.
  
  
  RESULTS
  The amounts of PPARα, carnitine palmitoyltransferase 1A and glyceraldehyde 3-phosphate dehydrogenase mRNA in cancerous sections were significantly increased compared to those in non-cancerous sections. The level of cyclin D1 mRNA tends to be higher in cancerous than non-cancerous sections. Although there was a significant correlation between the levels of PPARα mRNA and cyclin D1 mRNA in both sections, however the correlation was higher in cancerous sections.
  
  
  CONCLUSIONS
  The present investigation indicated increased expression of PPARα mRNA and mRNAs for PPARα target genes in human hepatocellular carcinoma. These results might be associated with its carcinogenesis and characteristic features of energy production.
authors.affiliation: Masuko Memorial Hospital, Takehashi-cho, Nakamura-ku, Nagoya, Japan. tsuyok@masuko.or.jp
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Kurokawa
authors.forename: Yoshiharu
authors.initials: Y
authors.lastname: Shimomura
authors.forename: Gustavo
authors.initials: G
authors.lastname: Bajotto
authors.forename: Katsuhiro
authors.initials: K
authors.lastname: Kotake
authors.forename: Takashi
authors.initials: T
authors.lastname: Arikawa
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Ito
authors.forename: Akira
authors.initials: A
authors.lastname: Yasuda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nagata
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Nonami
authors.forename: Kazuo
authors.initials: K
authors.lastname: Masuko
mesh_terms: D014408:Biomarkers, Tumor / Q000235:genetics*; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000473:pathology; D016022:Case-Control Studies; D019938:Cyclin D1 / Q000235:genetics; D006801:Humans; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008113:Liver Neoplasms / Q000235:genetics* / Q000473:pathology; D047493:PPAR alpha / Q000235:genetics*; D011379:Prognosis; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D014408:Biomarkers, Tumor; C530104:CCND1 protein, human; D047493:PPAR alpha; D012333:RNA, Messenger; D019938:Cyclin D1