PMID: 9434142Jan 20, 1998Paper

Tamoxifen inhibits the release of arachidonic acid stimulated by thapsigargin in estrogen receptor-negative A549 cells

Biochimica Et Biophysica Acta
J D CroxtallR J Flower

Abstract

In pre-labelled A549 cells the tumour promoter thapsigargin (50 nM) stimulates the release of [5,6,8,9,11,12,14,15-3H(N)]-arachidonic acid (3H-AA) by ca. 300% above basal levels. A549 cells are estrogen receptor negative (ER-), yet this stimulation by thapsigargin is inhibited in a dose-dependent manner by a 3 h pre-treatment with the anti-estrogen tamoxifen (1-20 microM). Moreover, the presence of excess (100 microM) estradiol does not reverse this effect of tamoxifen. Thapsigargin stimulated 3H-AA release is not inhibited over the same concentration range by 4 hydroxy-tamoxifen nor by the steroidal anti-estrogen ICI 164384. However, the steroidal anti-estrogen ICI 182780 inhibits thapsigargin stimulated 3H-AA release in a similar manner to tamoxifen and this effect is also not reversed by the presence of excess estradiol. Stimulation of 3H-AA release by EGF (10 nM), IL-1beta (1 ng ml-1) and bradykinin (100 nM) was unaffected by these concentrations of tamoxifen. Ionomycin (10 microM) stimulates 3H-AA release by ca. 700% and A23187 (10 microM) by ca. 300% above basal levels. Pre-treatment with tamoxifen (1-20 microM) inhibits 3H-AA release stimulated by both these agents and again the presence of excess estradiol does not reve...Continue Reading

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Citations

Apr 14, 1999·Proceedings of the National Academy of Sciences of the United States of America·N AltanS M Simon
Feb 20, 2013·The Journal of Physiology·Alina MarandykinaFeliksas F Bukauskas
Aug 26, 1998·International Journal of Cancer. Journal International Du Cancer·Y LavieM C Cabot
Jun 8, 2004·American Journal of Physiology. Lung Cellular and Molecular Physiology·Louise E DonnellyPeter J Barnes

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