ABSTRACT
Prolactin (PRL) is secreted by lactotrophs in the anterior pituitary and some extra-pituitary tissues such as breast, lacrimal gland, uterus, thymus and spleen, etc. Since PRL is closely related to growth hormone (GH) and placental lactogens (PL), it has been broadly accepted that PRL, GH and PL are resulted from the duplication of an ancestral gene. PRL regulates hundreds of biological functions by endocrine, paracrine and autocrine manners. Prolactin initiates its effects by binding to its receptor (PRLR). PRLR belongs to the class I cytokine receptor superfamily. Up to now, three membrane--PRLRs have been clarified. They are long form (LF), intermediate form (IF) and short form (SF) including SFla and SFlb. All PRLRs are derived from a primary transcript of common gene through alternative splicing mechanism. Although the extracellular domain (ECD) and the transmembrane domain (TD) of LF, IF and SF are equal, different isoforms of PRLR exert different function through different intracellular domain. It has been well documented that abnormity of PRLR is closely related to the pathogenesis, progression and prognosis of cancers including breast cancer. Several PRLR antagonists have been well designed and evidenced to have the potential to be important therapeutics.
