Tamoxifen Inhibits GH3 Cell Growth in Culture via Enhancement of Apoptosis

Tamoxifen Inhibits GH3 Cell Growth in Culture via Enhancement of Apoptosis 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurosurgery Oxford University Press

Tamoxifen Inhibits GH3 Cell Growth in Culture via Enhancement of Apoptosis

Tamoxifen Inhibits GH3 Cell Growth in Culture via Enhancement of Apoptosis

EXPERIMENTAL STUDIES Tamoxifen Inhibits G H 3 Cell Growth in Culture via Enhancement of Apoptosis So-Young Lee, M.S., Byung Tae Ahn, Ph.D., Sang-Ho Baik, M.D., Ph.D., Byung-Lan Lee, M.D., Ph.D. Department of Anatomy (S-YL, S-HB, B-LL), Seoul National University College of Medicine, Seoul, and Department of Biology (BTA), Catholic University, Bucheon, Korea O BJECTIVE: To investigate the antitumor effects of tamoxifen on pituitary tumor G H , cells, which lack receptors for dopamine. M ETHO DS: G H 3 cells were treated with tamoxifen (10“ mol/L), bromocriptine (1 0 “ H 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 5 3.0 % of that of untreated control cells. The percentage of PRL-immunoreactive G H } 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 /3-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 G H , cells to bromocriptine treatment. C O N C L U S IO N : Tamoxifen, an antiestrogen, exerts its antitumor effect on G H , cells in two ways: by suppression of cell growth and by causing a decrease in PRL. Apoptosis seems to contribute to the inhibition of G H , cell growth. (Neurosurgery 43:11 6 - 1 2 3 , 1998) Key words: Apoptosis, Cell growth, G H } cells, Prolactin,...
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Publisher
Congress of Neurological Surgeons
Copyright
© Published by Oxford University Press.
ISSN
0148-396X
eISSN
1524-4040
D.O.I.
10.1097/00006123-199807000-00076
Publisher site
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Abstract

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.

Journal

NeurosurgeryOxford University Press

Published: Jul 1, 1998

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