Recent studies have reported that, like 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), interleukin-1α inhibits 17β-estradiol-induced cell proliferation and [3H]thymidine uptake and also causes a downregulation of the nuclear estrogen receptor (ER)-positive MCF-7 human breast cancer cells. These results suggest a possible relationship between TCDD and interleukin-1α in human breast cancer cells. After treatment of MCF-7 cells with 1 nM TCDD, the media was changed every 48 hours over a period of 7 days and used to support the growth of cells which were not treated with TCDD. The results showed that media from cells treated with TCDD did not inhibit the growth of control or 17β-estradiol-treated MCF-7 cells. These results suggested that MCF-7 cells exposed to TCDD did not secrete anti-growth factors into the media. In a separate study, the media from control cells and those treated with 1 nM 17β-estradiol, 1 nM TCDD and 17β-estradiol plus TCDD were analyzed for interleukin-1α using commercially-available antibodies. The results showed that interleukin-1α was not detectable in media from any of the treatment groups and indicate that although interleukin-1α and TCDD cause several common responses in ER-positive human breast cancer cell lines, their modes of action are independent.
|Original language||English (US)|
|Number of pages||4|
|State||Published - 1992|
ASJC Scopus subject areas
- Environmental Engineering
- Environmental Chemistry
- Health, Toxicology and Mutagenesis