AbstractOBJECTIVE:To investigate the antitumor effects of tamoxifen on pituitary tumor GH3 cells, which lack receptors for dopamine.METHODS:GH3 cells were treated with tamoxifen (10−7 mol/L), bromocriptine (10−8 mol/L), or a combination of tamoxifen and bromocriptine in serum-free media. The cell number, bromodeoxyuridine (BrdU) labeling ratio, and apoptotic ratio were assessed. Prolactin (PRL) expression was examined using immunocytochemistry and Western blot analysis.RESULTS:After tamoxifen treatment for 4 days, the cell number decreased to 53.0% of that of untreated control cells. The percentage of PRL-immunoreactive GH3 cells decreased to 2.9%, versus 8.6% of untreated control cells, which was compatible with the results of Western blot analysis for PRL. Apoptosis increased to approximately three times that of untreated control cells at Day 2 of treatment, whereas no significant change was shown in BrdU incorporation. These effects by tamoxifen were not observed in the simultaneous treatment with 17 β-estradiol. Bromocriptine did not change the cell number, BrdU incorporation, the apoptotic ratio, or the percentage of PRL-positive cells, and it was also shown that tamoxifen did not change the sensitivity of GH, cells to bromocriptine treatment.CONCLUSION:Tamoxifen, an antiestrogen, exerts its antitumor effect on GH3 cells in two ways: by suppression of cell growth and by causing a decrease in PRL. Apoptosis seems to contribute to the inhibition of GH3 cell growth.
Neurosurgery – Oxford University Press
Published: Jul 1, 1998
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