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Istituto di Patologia Generate e Oncologia, Prima Facoltà di Medicina e Chirurgia Università di Napoli Napoli I-80138, Italy
Address requests for reprints to: Dr. Alessandro Weisz, Istituto di Patologia Generale e Oncologia, Prima Facolta di Medicina e Chirurgia, Università di Napoli, Piazza S. Andrea delle Dame, 2, Napoli 1-80138, Italy.
Abstract
Estrogen is a mitogen for the rat uterus, where it induces transient activation of c-fos and c-myc protooncogene expression, followed by increases in DNA synthesis and cell proliferation. JUN-C, the product of the c-jun protooncogene, is a nuclear protein that can interact with FOS to modulate the activity of AP-1 -responsive promoters. To test whether c-jun is a target for estrogen regulation, we measured the effects of 17β-estradiol on the expression of this gene in rat uterus. A human c-jun cDNA probe detects in rat uterus two mRNA species of 2.5 and 3.2 kilobases. Treatment of the animals with estrogen results in a rapid transient increase in the concentrations of these mRNAs; a 4- to 5-fold increase over the prestimulation level was detected starting 30 min after estrogen injection and lasting for 2 h, with a return to the prestimulation level after 4 h. In accordance with the results obtained by analysis of the mRNA, we found that estrogen increases 3- to 4-fold c-jun gene transcription in the uterus, at the same time it induces its mRNA accumulation. The ability of estrogen to induce c-jun gene expression was not abolished by the protein synthesis inhibitor cycloheximide, suggesting that transcriptional activation of this protooncogene is a primary response to the hormone. Furthermore, we found that in the estrogen-responsive MCF-7 human mammary carcinoma cells, estrogen stimulates transcription of a reporter gene containing four copies of a jun/AP-1 response element. These data demonstrate that c-jun gene expression is regulated by estrogen and suggest that JUN-C could play a role in the activation of cell proliferation by estrogen.
FOOTNOTES
This work was supported by grants from the Italian Ministry for Public Education (MPI), the Italian National Council for Research (CNR; Contract 00547.44), and the AIRC.
* EMBO Fellow in the Laboratoire de Génetique Moléculaire des Eukaryotes du CNRS, Unité 184 de Biologie Moléculaire et de Génie Génétique de l'INSERM, Faculté de Médecine, Université de Strasbourg, France, where part of the work was carried out.
Fellow of the Italian Association for Research on Cancer (AIRC).
Received for publication February 15, 1990. Revision received April 16, 1990. Accepted for publication April 19, 1990.
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