title: Regulation of PTP1D mRNA by peptide growth factors in the human endometrial cell line HEC-1-A.
abstract: OBJECTIVE
  To assess, in the human endometrial cell line HEC-1-A, the presence of protein tyrosine phosphatase 1D (PTP1D) and the possible regulation of its mRNA expression by mitogens such as forskolin (an agent that increases intracellular cyclic adenosine monophosphate [cAMP] levels), epidermal growth factor (EGF), and insulin-like growth factor-I (IGF-I).
  
  
  METHODS
  Cells were grown to confluence and maintained in serum-free media for 24 hours before treatment. Cells were exposed to forskolin, EGF, and IGF-I for increasing time periods (0, 1, 3, 6, and 24 hours), and PTP1D mRNA expression was determined by Northern blot analysis. In addition, cells were incubated with increasing doses of forskolin (final concentrations: 1, 5, 10, 20, and 30 mumol/L) for 6 hours.
  
  
  RESULTS
  When treated with the various mitogens, cells increased their stimulation of PTP1D mRNA expression in a time- and dose-dependent fashion. Specifically, forskolin, EGF, and IGF-I induced maximal mRNA expression at 6, 3, and 6 hours, respectively. Expression induced by forskolin, EGF, and IGF-I was five, three, and six times control levels, respectively. At a dose of 10 mumol/L, forskolin induced PTP1D mRNA expression almost two times higher than control values.
  
  
  CONCLUSIONS
  These data suggest that in human endometrial carcinomas, cAMP, EGF, and IGF-I may regulate the expression of PTP1D mRNA, which may, in turn, play a role in uncontrolled cell proliferation and neoplastic transformation.
authors.affiliation: Department of Obstetrics and Gynecology, University of Michigan Medical Center, Ann Arbor 48109-0617, USA.
authors.forename: J J
authors.initials: JJ
authors.lastname: Burke
authors.forename: F
authors.initials: F
authors.lastname: Talavera
authors.forename: K M
authors.initials: KM
authors.lastname: Menon
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology; D015152:Blotting, Northern; D002455:Cell Division / Q000187:drug effects; D002471:Cell Transformation, Neoplastic / Q000187:drug effects; D005576:Colforsin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D016889:Endometrial Neoplasms / Q000737:chemistry* / Q000378:metabolism / Q000473:pathology*; D004815:Epidermal Growth Factor / Q000494:pharmacology / Q000502:physiology; D005260:Female; D006133:Growth Substances / Q000494:pharmacology*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology / Q000502:physiology; D047908:Intracellular Signaling Peptides and Proteins; D054592:Protein Tyrosine Phosphatase, Non-Receptor Type 11; D053824:Protein Tyrosine Phosphatase, Non-Receptor Type 6; D017027:Protein Tyrosine Phosphatases / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D013997:Time Factors; D014407:Tumor Cells, Cultured
chemical_list: D006133:Growth Substances; D047908:Intracellular Signaling Peptides and Proteins; D012333:RNA, Messenger; D005576:Colforsin; D004815:Epidermal Growth Factor; D007334:Insulin-Like Growth Factor I; C516724:PTPN11 protein, human; C509249:PTPN6 protein, human; D054592:Protein Tyrosine Phosphatase, Non-Receptor Type 11; D053824:Protein Tyrosine Phosphatase, Non-Receptor Type 6; D017027:Protein Tyrosine Phosphatases