Abstract
Prolactin (PRL) is a hormone produced by the pituitary gland and multiple non-pituitary sites, vital in several physiological processes such as lactation, pregnancy, cell growth, and differentiation. However, PRL is nowadays known to have a strong implication in oncogenic processes, making it essential to delve into the mechanisms governing these actions. PRL and its receptor (PRLR) activate a series of effects such as survival, cellular proliferation, migration, invasion, metastasis, and resistance to treatment, being highly relevant in developing certain types of cancer. Because women produce high levels of PRL, its influence in gynecological cancers is herein reviewed. It is interesting that, other than the 23 kDa PRL, whose mechanism of action is endocrine, other variants of PRL have been observed to be produced by tumoral tissue, acting in a paracrine/autocrine manner. Because many components, including PRL, surround the microenvironment, it is interesting to understand the hormone’s modulation in cancer cells. This work aims to review the most important findings regarding the PRL/PRLR axis in cervical, ovarian, and endometrial cancers and its molecular mechanisms to support carcinogenesis.
Highlights
Prolactin (PRL), belonging to the PRL/growth hormone (GH)/placental lactogen family, is a polypeptide and pleiotropic hormone but mainly recognized as a lactogenic hormone and is primarily synthesized and secreted from the lactotroph cells of the anterior pituitary gland [1,2,3,4,5]
We analyze these findings, and we present the current panorama of research on PRL-prolactin receptor (PRLR) and its effects on gynecological cancers and the perspectives on the use of PRL as a therapeutic target
The PRLR has been found widely expressed in the cervix, ovary, and endometrium cancers compared to their healthy tissues
Summary
Prolactin (PRL), belonging to the PRL/growth hormone (GH)/placental lactogen family, is a polypeptide and pleiotropic hormone but mainly recognized as a lactogenic hormone and is primarily synthesized and secreted from the lactotroph cells of the anterior pituitary gland [1,2,3,4,5]. PRL is synthesized in multiple non-pituitary sites, including the endometrium, Prolactin in Gynecological Cancers myometrium, decidua, immune cells, brain, breast, prostate, skin, and adipose tissue [2,3,4,5,6], acting as a paracrine/autocrine signaling molecule [5], and locally as a growth-promoting factor [2, 3, 7]. The interaction between PRL and the prolactin receptor (PRLR) mainly promotes protumoral events, such as migration, invasion, metastasis, chemoresistance, inhibition of apoptosis, among others, through the activation of different signaling pathways and effector proteins, which will be addressed later. We analyze these findings, and we present the current panorama of research on PRL-PRLR and its effects on gynecological cancers and the perspectives on the use of PRL as a therapeutic target
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