2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) inhibits human ovarian cancer cell proliferation.

摘要: The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, mediates broad spectrum of biological processes, including ovarian growth and ovulation. Recently, we found that an endogenous AhR ligand (ITE) can inhibit cancer proliferation migration via the AhR. Here, tested whether 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, exogenous ligand) may exert similar anti-ovarian activities using human non-cancerous surface epithelial cells. Two cell lines (SKOV-3 OVCAR-3) one line (IOSE-385) were used. Cell determined crystal violet FluoroBlok insert system assays, respectively. protein expression was assessed by Western blotting. Expression cytochrome P450, family 1, member A1 (CYP1A1) B1 (CYP1B1) mRNA qPCR. Small interfering RNAs (siRNAs) used to knock down expression. We TCDD dose-dependently suppressed OVCAR-3 proliferation, with maximum effect (~70 % reduction) at 100 nM. However, did not affect SKOV-3 IOSE-385 migration. estimated IC50 for inhibiting 4.6 At 10 nM, time-dependently decreased levels, while it significantly increased CYP1A1 CYP1B1 levels in SKOV-3, cells, indicating activation signaling. siRNA-mediated knockdown readily blocked TCDD-mediated suppression proliferation. Our data indicate suppress signaling pathway exhibits anti-proliferative activity least subset