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Prolactin (PRL) is a hormone synthesized by lactotrophs in the anterior pituitary gland. It is also produced by extrapituitary glands such as the prostate and breast, where it promotes growth. Notably, PRL also contributes to cancer development in these glands. PRL is known to stimulate cancer cell migration, suggesting its possible involvement in metastasis, for which cell migration is a critical step. However, the role and mechanisms by which PRL induces cancer cell migration are not yet fully understood. One well-studied mechanism involves its receptor, the prolactin receptor (PRLR). After PRL binds to its receptor, PRLR dimerizes and induces transphosphorylation of Janus kinase 2 (JAK2), which subsequently phosphorylates p21-activated kinase 1 (PAK1), leading to increased cell migration. Although the PRL-JAK2-PAK1 pathway in cancer cell migration has been investigated, the molecular mechanism remains incompletely understood. Additionally, other PRL-activated pathways are implicated in migration, but their roles remain debated. This narrative review examines and discusses the main findings on the involvement of PRL in the migration of cancerous and non-cancerous cells, as well as the molecular mechanisms involved. We conclude that PRL promotes the migration of both cancerous and non-cancerous cell lines and should, therefore, be taken into account in future cancer research.
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Jiménez-Buendía et al. (2026) studied this question.
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