New mechanisms for PRLr action in breast cancer

Charles V. Clevenger*, Samantha L. Gadd, Jiamao Zheng

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

66 Scopus citations

Abstract

Prolactin (PRL) is a pleiotrophic hormone that contributes to the growth of normal and malignant breast tissues. PRL signals through its receptor (PRLr), a transmembrane receptor that belongs to the cytokine receptor family. The mechanism of how the PRL:PRLr interaction triggers activation of signaling networks remains enigmatic. This review examines the effect of ligand binding on PRLr and the processes that initiate receptor-associated signaling. Evidence for PRLr predimerization in the absence of ligand and the actions of the prolyl isomerase cyclophilin A in ligand-induced activation of PRLr-associated Jak2 kinase are discussed. These studies reveal that ligand-induced conformational change of the PRLr complex is necessary for its function and open avenues for therapies to inhibit PRLr action in breast cancer.

Original languageEnglish (US)
Pages (from-to)223-229
Number of pages7
JournalTrends in Endocrinology and Metabolism
Volume20
Issue number5
DOIs
StatePublished - Jul 1 2009

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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