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Journal of the Society for Gynecologic Investigation
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Regulation of PTP1D mRNA by Peptide Growth Factors in the Human Endometrial Cell Line HEC-1-A

James J. Burke, II, MD

Francisco Talavera, PhD

Department of Obstetrics and Gynecology, University of Michigan Medical Center, Ann Arbor, Michigan

K. M. J. Menon, PhD

Department of Obstetrics and Gynecology, University of Michigan Medical Center, 6428 Med Sci 1, 1301 Catherine Street, Ann Arbor, MI 48109-0617

Objective: To assess, in the human endometrial cell line HEC-1-A, the presence of protein tyrosine phosphatase 1D (PTDP1D) 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 µmol/L0 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 µmol/L, forskolin induced PTP1D mRNA expression almost two times higher than control values.

Conclusion: 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.

Key Words: Peptide growth factors • PTP1D • EGF • IGF-I • forskolin • cAMP • HEC-1A

Journal of the Society for Gynecologic Investigation, Vol. 4, No. 6, 310-315 (1997)
DOI: 10.1177/107155769700400608
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