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

91 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 2009

Funding

This work was supported by the Susan G. Komen Foundation BCTR05–03790 and NIH grants CA69294 and CA102682. Additional support was received from the Zell Scholar's Fund, the Lynn Sage Foundation and the Avon Foundation. J.Z. was supported by a Department of Defense Multidisciplinary Postdoctoral Award BC073498.

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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