S Y Lee1, B T Ahn, S H Baik, B L Lee. 1. Department of Anatomy, Seoul National University College of Medicine, Korea.
Abstract
OBJECTIVE: 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 17beta-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 GH3 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.
OBJECTIVE: 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 17beta-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 GH3 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.
Authors: Bin Huang; Nao Luo; Xinhao Wu; Zhixiang Xu; Xiaoxia Wang; Xuejun Pan Journal: Environ Sci Pollut Res Int Date: 2018-11-22 Impact factor: 4.223
Authors: B Voellger; N Waldt; Rosita Rupa; E Kirches; O Melhem; H-J Ochel; C Mawrin; R Firsching Journal: J Neurooncol Date: 2018-06-05 Impact factor: 4.130