中文摘要：

Background Prolactin （PRL） is a pituitary polypeptide hormone characterized by multiple biological actions includingstimulation of growth in the prostate and formation of secretory alveoli and stimulation of milk protein gene expression inthe mammary gland. PRL exerts its effect by dimerizing its receptor （PRLR） on the plasma membrane and regulating geneexpression through the JAK-Stat signal pathway. We have previously described a natural variant of the PRLR in which the$2 subdomain of the extracellular domain is missing （Delta S2）. Delta S2 PRLRs are dimerized in the absence of PRL andhave constitutive activity in the promotion of breast cancer cell growth. Enhancer of zeste homolog 2 （EZH2）, as one of thehistone-modifying enzymes, is a key factor regulating gene expression by epigenetic modification. We hypothesized thatthese constitutive activated Delta S2 PRLRs played a pathogenic role in breast cancer in part through alterations in theexpression of EZH2 and the trimethylation of histone 3 on lysine 27 （H3K27Me3）.