RT Journal Article
SR Electronic
T1 Delta(9)-tetrahydrocannabinol Inhibits 17β-Estradiol-induced Proliferation and Fails to Activate Androgen and Estrogen Receptors in MCF7 Human Breast Cancer Cells
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 85
OP 89
VO 28
IS 1A
A1 A. O. VON BUEREN
A1 M. SCHLUMPF
A1 W. LICHTENSTEIGER
YR 2008
UL http://ar.iiarjournals.org/content/28/1A/85.abstract
AB Background: Delta(9)-tetrahydrocannabinol (THC) exerts palliative effects in cancer patients, but produces adverse effects on the endocrine and reproductive systems. Experimental evidence concerning such effects is controversial. Whether THC exhibits estrogenic or androgenic activity in vitro was investigated. Materials and Methods: Estrogenic effects of THC were analyzed in vitro by measuring the proliferation of estrogen-sensitive MCF7 cells. Androgenic activity was investigated by the A-Screen assay that measures androgen-dependent inhibition of proliferation of the androgen receptor (AR)-positive human mammary carcinoma cell line, MCF7-AR1. Results: In contrast to 17β-estradiol, included as positive control with an EC50 value (concentration required for 50% of maximal 17β-estradiol-induced proliferation) of 1.00×10-12 M, THC failed to induce cell proliferation in the MCF7 cell line at concentrations between 10-13 and 10-4 M. THC inhibited 17β-estradiol-induced proliferation in wild-type MCF7 and MCF7-AR1 cells, with an IC50 value of 2.6×10-5 M and 9×10-6 M, respectively. Conclusion: THC failed to act as an estrogen, but antagonized 17β-estradiol-induced proliferation. This effect was independent of the AR expression level.