New mechanisms for PRLr action in breast cancer

Charles V. Clevenger; Samantha L. Gadd; Jiamao Zheng

doi:10.1016/j.tem.2009.03.001

New mechanisms for PRLr action in breast cancer

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

^*Corresponding author for this work

Pathology

Research output: Contribution to journal › Review article › peer-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 language	English (US)
Pages (from-to)	223-229
Number of pages	7
Journal	Trends in Endocrinology and Metabolism
Volume	20
Issue number	5
DOIs	https://doi.org/10.1016/j.tem.2009.03.001
State	Published - 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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.tem.2009.03.001

Cite this

@article{3bfbee464cc247149391cc366f08701b,

title = "New mechanisms for PRLr action in breast cancer",

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.",

author = "Clevenger, {Charles V.} and Gadd, {Samantha L.} and Jiamao Zheng",

note = "Funding Information: 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.",

year = "2009",

month = jul,

doi = "10.1016/j.tem.2009.03.001",

language = "English (US)",

volume = "20",

pages = "223--229",

journal = "Trends in Endocrinology and Metabolism",

issn = "1043-2760",

publisher = "Elsevier Inc.",

number = "5",

}

TY - JOUR

T1 - New mechanisms for PRLr action in breast cancer

AU - Clevenger, Charles V.

AU - Gadd, Samantha L.

AU - Zheng, Jiamao

N1 - Funding Information: 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.

PY - 2009/7

Y1 - 2009/7

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=67649216555&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67649216555&partnerID=8YFLogxK

U2 - 10.1016/j.tem.2009.03.001

DO - 10.1016/j.tem.2009.03.001

M3 - Review article

C2 - 19535262

AN - SCOPUS:67649216555

SN - 1043-2760

VL - 20

SP - 223

EP - 229

JO - Trends in Endocrinology and Metabolism

JF - Trends in Endocrinology and Metabolism

IS - 5

ER -

New mechanisms for PRLr action in breast cancer

Abstract

Funding

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this