Tamoxifen (ICI 46474, (Z)-Tamoxifen, trans-Tamoxifen) is a selective estrogen receptor modulator (SERM). Tamoxifen enhances the Hsp90 molecular chaperone ATPase activity. Tamoxifen induces apoptosis.
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Tamoxifen (ICI 46474, (Z)-Tamoxifen, trans-Tamoxifen) is a selectiveestrogen receptormodulator (SERM). Tamoxifen enhances theHsp90molecular chaperoneATPaseactivity. Tamoxifen inducesapoptosis. In vitro
TAM treatment inhibits significantly MCF7 cell proliferation. Low doses of TAM are able to induce structural chromosomal aberrations (deletions, isochromosomes, translocations, and dicentric chromosomes) in both ER+ and ER- breast cancer cells. This genotoxic effect is higher in those cell lines with HER2 gene amplification. Whereas TAM at lower concentrations (0.1-1 μM) induces a cell-cycle arrest, pharmacological concentrations (above 5 μM) of TAM have been found to induce apoptosis of breast cancer cells. 5 μM TAM rapidly induced sustained activation of ERK1/2 in ER-positive breast cancer cell lines (MCF-7 and T47D)
In vivo
Tamoxifen (TAM) is widely used for both treatment and prevention of breast cancer. However, it is also carcinogenic in human uterus and rat liver. Tm-inducible Cre-loxP systems are being used in broad areas of research and are providing important biologic insights in tissue development, maintenance, and function. Tamoxifen-induced nuclear localization of Cre recombinase is time- and dose-dependent. Higher doses of tamoxifen induce recombination weeks following administration and Lower doses of tamoxifen induce recombination up to one week following administration. Duration of tamoxifen-induced gene recombination is also dose-dependent. Administration of high Tm doses leads to extended CreER nuclear localization. Tm treatment induces side effects that may have physiologic consequences in Tm-inducible models. Cell Data
cell lines：CLL B cells or healthy volunteer T cells or NK cells
