Effect of 17-beta Estradiol on the Expression of Inducible Nitric oxide Synthase in Parent and Tamoxifen Resistant T47D Breast Cancer Cells

Indirect evidence suggests that estrogen is involved in the etiology of breast cancer. estrogen is also thought to modulate nitric oxide (no) in human breast tumor tissue via regulation of inducible nitric oxide synthase (inos). objectives of this study were to determine whether estradiol (e2) affects inos expression level in breast cancer cells and to study the effect of various concentrations of e2 on cell proliferation. immunocytochemical technique was employed to assess inos expression level. proliferation of parent and 10-6 m tamoxifen resistant cells (t47d/tamr-6) were assessed by mtt assay in the presence of e2. addition of e2 (10-12 to 10-8 m) increases the expression of inos in parent cells, but not t47d/tamr-6, further increase in concentrations of e2 (10-8 to 10-4 m) again decreases the expression of inos in parent cells, but increase that of the t47d/tamr-6 cells. expression of inos in parent cells in a medium containing 1% serum (low serum) is less than the cells grown in a medium containing 10% fbs (normal serum). this trend was not seen in t47d/tamr-6 cells. the results of these experiments may indicate that increasing of inos expression decreases the viability of parent cells whilst increasing the number of t47d/tamr-6.