Lactation opposes pappalysin‐1‐driven pregnancy‐associated breast cancer

Abstract Pregnancy is associated with a transient increase in risk for breast cancer. However, the mechanism underlying pregnancy‐associated breast cancer (PABC) is poorly understood. Here, we identify the protease pappalysin‐1 (PAPP‐A) as a pregnancy‐dependent oncogene. Transgenic expression of PAP...

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Main Authors: Yukie Takabatake, Claus Oxvig, Chandandeep Nagi, Kerin Adelson, Shabnam Jaffer, Hank Schmidt, Patricia J Keely, Kevin W Eliceiri, John Mandeli, Doris Germain
Format: Article
Language:English
Published: Springer Nature 2016-03-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.201606273
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author Yukie Takabatake
Claus Oxvig
Chandandeep Nagi
Kerin Adelson
Shabnam Jaffer
Hank Schmidt
Patricia J Keely
Kevin W Eliceiri
John Mandeli
Doris Germain
author_facet Yukie Takabatake
Claus Oxvig
Chandandeep Nagi
Kerin Adelson
Shabnam Jaffer
Hank Schmidt
Patricia J Keely
Kevin W Eliceiri
John Mandeli
Doris Germain
author_sort Yukie Takabatake
collection DOAJ
description Abstract Pregnancy is associated with a transient increase in risk for breast cancer. However, the mechanism underlying pregnancy‐associated breast cancer (PABC) is poorly understood. Here, we identify the protease pappalysin‐1 (PAPP‐A) as a pregnancy‐dependent oncogene. Transgenic expression of PAPP‐A in the mouse mammary gland during pregnancy and involution promotes the deposition of collagen. We demonstrate that collagen facilitates the proteolysis of IGFBP‐4 and IGFBP‐5 by PAPP‐A, resulting in increased proliferative signaling during gestation and a delayed involution. However, while studying the effect of lactation, we found that although PAPP‐A transgenic mice lactating for an extended period of time do not develop mammary tumors, those that lactate for a short period develop mammary tumors characterized by a tumor‐associated collagen signature (TACS‐3). Mechanistically, we found that the protective effect of lactation is associated with the expression of inhibitors of PAPP‐A, STC1, and STC2. Collectively, these results identify PAPP‐A as a pregnancy‐dependent oncogene while also showing that extended lactation is protective against PAPP‐A‐mediated carcinogenesis. Our results offer the first mechanism that explains the link between breast cancer, pregnancy, and breastfeeding.
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spelling doaj-art-a3c1ba4b77a44936a9cd74d63af3b3d22025-08-20T03:46:16ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842016-03-018438840610.15252/emmm.201606273Lactation opposes pappalysin‐1‐driven pregnancy‐associated breast cancerYukie Takabatake0Claus Oxvig1Chandandeep Nagi2Kerin Adelson3Shabnam Jaffer4Hank Schmidt5Patricia J Keely6Kevin W Eliceiri7John Mandeli8Doris Germain9Division of Hematology/Oncology of the Icahn School of Medicine at Mount Sinai, Tisch Cancer InstituteDepartment of Molecular Biology and Genetics, Aarhus UniversityDepartment of Pathology of the Icahn School of Medicine at Mount Sinai, Tisch Cancer InstituteDubin Breast Center of the Icahn School of Medicine, Tisch Cancer InstituteDepartment of Pathology of the Icahn School of Medicine at Mount Sinai, Tisch Cancer InstituteDubin Breast Center of the Icahn School of Medicine, Tisch Cancer InstituteDepartment of Cell and Regenerative Biology, University of WisconsinLaboratory for Optical and Computational Instrumentation, University of WisconsinDepartment of Biostatistical Sciences, Icahn School of Medicine at Mount SinaiDivision of Hematology/Oncology of the Icahn School of Medicine at Mount Sinai, Tisch Cancer InstituteAbstract Pregnancy is associated with a transient increase in risk for breast cancer. However, the mechanism underlying pregnancy‐associated breast cancer (PABC) is poorly understood. Here, we identify the protease pappalysin‐1 (PAPP‐A) as a pregnancy‐dependent oncogene. Transgenic expression of PAPP‐A in the mouse mammary gland during pregnancy and involution promotes the deposition of collagen. We demonstrate that collagen facilitates the proteolysis of IGFBP‐4 and IGFBP‐5 by PAPP‐A, resulting in increased proliferative signaling during gestation and a delayed involution. However, while studying the effect of lactation, we found that although PAPP‐A transgenic mice lactating for an extended period of time do not develop mammary tumors, those that lactate for a short period develop mammary tumors characterized by a tumor‐associated collagen signature (TACS‐3). Mechanistically, we found that the protective effect of lactation is associated with the expression of inhibitors of PAPP‐A, STC1, and STC2. Collectively, these results identify PAPP‐A as a pregnancy‐dependent oncogene while also showing that extended lactation is protective against PAPP‐A‐mediated carcinogenesis. Our results offer the first mechanism that explains the link between breast cancer, pregnancy, and breastfeeding.https://doi.org/10.15252/emmm.201606273breastfeedingIGF‐binding protein 4 and 5insulin‐like growth (IGF) factor signalinginvolution
spellingShingle Yukie Takabatake
Claus Oxvig
Chandandeep Nagi
Kerin Adelson
Shabnam Jaffer
Hank Schmidt
Patricia J Keely
Kevin W Eliceiri
John Mandeli
Doris Germain
Lactation opposes pappalysin‐1‐driven pregnancy‐associated breast cancer
EMBO Molecular Medicine
breastfeeding
IGF‐binding protein 4 and 5
insulin‐like growth (IGF) factor signaling
involution
title Lactation opposes pappalysin‐1‐driven pregnancy‐associated breast cancer
title_full Lactation opposes pappalysin‐1‐driven pregnancy‐associated breast cancer
title_fullStr Lactation opposes pappalysin‐1‐driven pregnancy‐associated breast cancer
title_full_unstemmed Lactation opposes pappalysin‐1‐driven pregnancy‐associated breast cancer
title_short Lactation opposes pappalysin‐1‐driven pregnancy‐associated breast cancer
title_sort lactation opposes pappalysin 1 driven pregnancy associated breast cancer
topic breastfeeding
IGF‐binding protein 4 and 5
insulin‐like growth (IGF) factor signaling
involution
url https://doi.org/10.15252/emmm.201606273
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