Inhibition of Prolactin Receptor Gene Expression by 2,3,7,8-Tetrachlorodibenzo-p-dioxin in MCF-7 Human Breast Cancer Cells Academic Article uri icon

abstract

  • Treatment of MCF-7 human breast cancer cells with 10 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) did not decrease prolactin receptor (PRLR) binding. In contrast, PRLR mRNA levels were significantly decreased within 12 h after treatment with TCDD and persisted for up to 48 h. The effects of TCDD on PRLR mRNA levels were inhibited by the aryl hydrocarbon (Ah) receptor antagonist alpha-naphthoflavone and were not observed in Ah nonresponsive benzo[alpha]pyrene-resistant MCF-7 cells. These results suggest that the effects of TCDD were mediated through the Ah receptor. After treatment of MCF-7 cells with 10 nM 17 beta-estradiol (E2), there was a 2.3-fold increase in PRLR mRNA levels, and in cells cotreated with E2 plus TCDD, there was a 72% decrease in E2-induced PRLR mRNA levels. Previous studies have showed that TCDD also effects estrogen receptor (ER) binding and mRNA levels through the aryl hydrocarbon receptor pathway; however, the effects of TCDD on PRLR levels and binding in MCF-7 cells were different from those previously observed for ER.

author list (cited authors)

  • Lu, Y., Sun, G., Wang, X., & Safe, S.

citation count

  • 27

complete list of authors

  • Lu, YF||Sun, G||Wang, X||Safe, S

publication date

  • August 1996