Oxytocin (OT) inhibits the proliferation of MCF7 estrogen-dependent human breast cancer cells, via specific OT receptors (OTR). Besides this effect, we report that OT modulates the expression of estrogen receptor α (ERα) in MCF7 cells, both at mRNA and protein level. Since the first 24 h of OT treatment the ERα mRNA levels are down-regulated; in contrast, ERα protein expression decreases at a later time. The reduced number of ERα goes in parallel to a temporary increase in the binding affinity of these receptors as well as to a significant increase in their estradiol (E2)-induced trascription activity. The increase in both binding affinity and trascriptional activity of ERα likely balances the reduction in the number of ERα binding sites, ruling out the hypothesis that part of the OT contrasting effect on E2-induced cell proliferation could depend on the reduced E2 binding to MCF7 cells and supporting the hypothesis of an exclusively direct OT-antimitogenic effect. This is the first evidence that OT modulates the expression of ERα receptors in human neoplastic cells.

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