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MBC in Press, published online ahead of print September 5, 2003
Mol. Biol. Cell 10.1091/mbc.E03-05-0303

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Submitted on May 15, 2003
Revised on July 10, 2003
Accepted on July 25, 2003

Distinct Signaling Pathways Mediate Stimulation of Cell Cycle Progression and Prevention of Apoptotic Cell Death by Estrogen in Rat Pituitary Tumor PR1 Cells

Simona Caporali1, Manami Imai1, Lucia Altucci1, Massimo Cancemi1, Silvana Caristi1, Luigi Cicatiello1, Filomena Matarese1, Roberta Penta1, Dipak K. Sarkar2, Francesco Bresciani1, and Alessandro Weisz*

1 Dipartimento di Patologia generale, Seconda Università degli Studi di Napoli, Napoli, Italy
2 Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, USA

* Corresponding author. E-mail address: alessandro.weisz{at}unina2.it.

Estrogens control cell growth and viability in target cells via a interplay of genomic and extragenomic pathways not yet elucidated. Here we show evidence that cell proliferation and survival are differentially regulated by estrogen in rat pituitary tumor PR1 cells. Pico to femtomolar concentrations of 17{beta}-estradiol (E2) are sufficient to foster PR1 cell proliferation, whereas nanomolar concentrations of the same are needed to prevent cell death, that occurs at high rate in these cells in the absence of hormone. Activation of endogenous (PRL) or transfected estrogen-responsive genes occur at the same, higher concentrations of E2 required to promote cell survival, whereas stimulation of cyclin D3 expression and DNA synthesis occur at lower E2 concentrations. Similarly, the pure antiestrogen ICI 182,780 inhibits ERE-dependent trans-activation and cell death more effectively than cyclin-cdk activity, G1-S transition or DNA synthesis rate. In antiestrogen-treated and/or estrogen-deprived cells, death is due predominantly to apoptosis. Estrogen-induced cell survival, but not E2-dependent cell cycle progression, can be prevented by an inhibitor of c-Src kinase or by blockade of the MEK/ERK signaling pathway. These data indicate the coexistence of two distinguishable estrogen signaling pathways in PR1 cells, characterized by different functions and sensitivity to hormones and antihormones.




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