title: Selection of an internal control gene for quantitation of mRNA in colonic tissues.
abstract: BACKGROUND
  GAPDH, beta-actin and 18S rRNA are widely employed as internal control genes, with the assumption that they are expressed constitutively to similar degrees in different cells and tissues and under different experimental conditions. In this study, we tested this assumption by assessment of the transcription of these three genes in human colonic tissues using a quantitative RT-PCR.
  
  
  RESULTS
  GAPDH transcription was significantly greater in both colonic adenomas and cancers than in normal mucosa. In addition, transcription of beta-actin was significantly increased in cancers. The expression of 18S rRNA was essentially constant among these various tissues. Stable expression of 18S rRNA was observed during the growth of colonic cancer cells stimulated with serum, but both GAPDH and beta-actin transcription were up-regulated, coinciding with cell proliferation.
  
  
  CONCLUSIONS
  These results indicate that 18S rRNA is more reliable than GAPDH and beta-actin as an internal control gene for quantitative comparison of mRNA in colonic cancers.
authors.affiliation: Department of Clinical Laboratory Medicine and Division of Laboratory Diagnosis, Sapporo Medical University, School of Medicine, Sapporo, Japan.
authors.forename: Naoki
authors.initials: N
authors.lastname: Tsuji
authors.forename: Chinatsu
authors.initials: C
authors.lastname: Kamagata
authors.forename: Momoko
authors.initials: M
authors.lastname: Furuya
authors.forename: Daisuke
authors.initials: D
authors.lastname: Kobayashi
authors.forename: Atsuhito
authors.initials: A
authors.lastname: Yagihashi
authors.forename: Takayuki
authors.initials: T
authors.lastname: Morita
authors.forename: Shoichi
authors.initials: S
authors.lastname: Horita
authors.forename: Naoki
authors.initials: N
authors.lastname: Watanabe
mesh_terms: D000199:Actins / Q000096:biosynthesis / Q000235:genetics*; D000230:Adenocarcinoma / Q000235:genetics* / Q000378:metabolism; D000236:Adenoma / Q000235:genetics* / Q000378:metabolism; D003106:Colon / Q000378:metabolism / Q000502:physiology; D003110:Colonic Neoplasms / Q000235:genetics* / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000096:biosynthesis / Q000235:genetics*; D019073:HT29 Cells; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism / Q000502:physiology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics*; D012337:RNA, Ribosomal, 18S / Q000096:biosynthesis / Q000235:genetics*; D014158:Transcription, Genetic; D014407:Tumor Cells, Cultured
chemical_list: D000199:Actins; D012333:RNA, Messenger; D012337:RNA, Ribosomal, 18S; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases