title: AKT-1, -2, and -3 are expressed in both normal and tumor tissues of the lung, breast, prostate, and colon.
abstract: OBJECTIVE
  The AKT/PKB kinase controls many of the intracellular processes that are dysregulated in human cancer, including the suppression of apoptosis and anoikis and the induction of cell cycle progression. Three isoforms of AKT have been identified: AKT-1, -2, and -3. Selective up-regulation of AKT-3 RNA expression has been reported in hormone-independent breast and prostate cancer cell lines suggesting that AKT-3 expression may be increased with breast or prostate tumor progression. To determine whether AKT-3 RNA expression is selectively up-regulated in human cancers and whether the patterns of AKT RNA expression may change with tumor development, we examined AKT isoform expression by RT-PCR in human cancer cell lines, primary human cancers, and normal human tissues.
  
  
  METHODS
  AKT-1, -2, and -3 RNA expression was examined by RT-PCR. Because up-regulated AKT-3 expression has been implicated in human breast and prostate cancer progression, we also examined AKT-3 expression levels by semiquantitative RT-PCR using matched normal/tumor first-strand cDNA pairs from colon, breast, prostate, and lung cancers.
  
  
  RESULTS
  Our data reveal that the overwhelming majority of both normal and tumor tissues express all three of the AKT isoforms. Moreover, semiquantitative RT-PCR of matched normal/tumor pairs confirmed similar AKT-3 RNA expression levels in both normal and tumor tissue.
  
  
  CONCLUSIONS
  Our data show that both normal and tumor tissues express all three of the AKT isoforms and indicate that tumorigenesis does not involve a dramatic shift in the RNA expression patterns of the three AKT isoforms.
authors.affiliation: Cancer Research Division, Lilly Research Labs, Eli Lilly and Company, Lilly Corporate Center DC 0546, Indianapolis, IN 46285, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: Zinda
authors.forename: M A
authors.initials: MA
authors.lastname: Johnson
authors.forename: J D
authors.initials: JD
authors.lastname: Paul
authors.forename: C
authors.initials: C
authors.lastname: Horn
authors.forename: B W
authors.initials: BW
authors.lastname: Konicek
authors.forename: Z H
authors.initials: ZH
authors.lastname: Lu
authors.forename: G
authors.initials: G
authors.lastname: Sandusky
authors.forename: J E
authors.initials: JE
authors.lastname: Thomas
authors.forename: B L
authors.initials: BL
authors.lastname: Neubauer
authors.forename: M T
authors.initials: MT
authors.lastname: Lai
authors.forename: J R
authors.initials: JR
authors.lastname: Graff
mesh_terms: D001940:Breast / Q000378:metabolism / Q000473:pathology; D001943:Breast Neoplasms / Q000235:genetics / Q000473:pathology; D003106:Colon / Q000378:metabolism / Q000473:pathology; D003110:Colonic Neoplasms / Q000235:genetics / Q000473:pathology; D005260:Female; D015870:Gene Expression; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008175:Lung Neoplasms / Q000235:genetics / Q000473:pathology; D008297:Male; D009369:Neoplasms / Q000235:genetics* / Q000473:pathology; D015513:Oncogene Proteins / Q000235:genetics; D011467:Prostate / Q000378:metabolism / Q000473:pathology; D011471:Prostatic Neoplasms / Q000235:genetics / Q000473:pathology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D051057:Proto-Oncogene Proteins c-akt; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014018:Tissue Distribution; D014407:Tumor Cells, Cultured
chemical_list: D015513:Oncogene Proteins; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D012334:RNA, Neoplasm; C494918:AKT1 protein, human; C491754:AKT3 protein, human; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt