Desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen

Abstract Full term pregnancy at an early age is the only factor known to consistently protect against breast cancer. Because hormone receptor positive progenitors in the human breast relay endocrine signaling, we here sought to determine whether an experimental mimicry of the third trimester surge o...

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Autores principales:	Lone Rønnov-Jessen, Jiyoung Kim, Nadine Goldhammer, Marie Christine Klitgaard, Martynas Smicius, Marc Baker Bechmann, René Villadsen, Ole William Petersen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9d1066b65c1f4879aa2a803d4e53a46b
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spelling	oai:doaj.org-article:9d1066b65c1f4879aa2a803d4e53a46b2021-12-02T19:02:27ZDesensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen10.1038/s41598-021-96785-82045-2322https://doaj.org/article/9d1066b65c1f4879aa2a803d4e53a46b2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-96785-8https://doaj.org/toc/2045-2322Abstract Full term pregnancy at an early age is the only factor known to consistently protect against breast cancer. Because hormone receptor positive progenitors in the human breast relay endocrine signaling, we here sought to determine whether an experimental mimicry of the third trimester surge of hormones would change their susceptibility to growth stimulation. Hormone receptor positive, reduction mammoplasty-derived human breast epithelial progenitors were exposed to a short-term, pregnancy-level of estradiol, and their subsequent response to estradiol stimulation was analyzed. Exposure to pregnancy-level of estradiol results in subsequent lower sensitivity to estrogen-induced proliferation. Expression array and immunoblotting reveal upregulation of S100A7 and down-regulation of p27, both associated with parity and epithelial differentiation. Notably, we find that the epithelial differentiation is accompanied by upregulation of E-cadherin and down-regulation of vimentin as well as by diminished migration and more mature luminal epithelial differentiation in a mouse transplantation model. Our findings are in support of a de-sensitization mechanism for pregnancy-induced prevention against breast cancer.Lone Rønnov-JessenJiyoung KimNadine GoldhammerMarie Christine KlitgaardMartynas SmiciusMarc Baker BechmannRené VilladsenOle William PetersenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-7 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Lone Rønnov-Jessen Jiyoung Kim Nadine Goldhammer Marie Christine Klitgaard Martynas Smicius Marc Baker Bechmann René Villadsen Ole William Petersen Desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen
description	Abstract Full term pregnancy at an early age is the only factor known to consistently protect against breast cancer. Because hormone receptor positive progenitors in the human breast relay endocrine signaling, we here sought to determine whether an experimental mimicry of the third trimester surge of hormones would change their susceptibility to growth stimulation. Hormone receptor positive, reduction mammoplasty-derived human breast epithelial progenitors were exposed to a short-term, pregnancy-level of estradiol, and their subsequent response to estradiol stimulation was analyzed. Exposure to pregnancy-level of estradiol results in subsequent lower sensitivity to estrogen-induced proliferation. Expression array and immunoblotting reveal upregulation of S100A7 and down-regulation of p27, both associated with parity and epithelial differentiation. Notably, we find that the epithelial differentiation is accompanied by upregulation of E-cadherin and down-regulation of vimentin as well as by diminished migration and more mature luminal epithelial differentiation in a mouse transplantation model. Our findings are in support of a de-sensitization mechanism for pregnancy-induced prevention against breast cancer.
format	article
author	Lone Rønnov-Jessen Jiyoung Kim Nadine Goldhammer Marie Christine Klitgaard Martynas Smicius Marc Baker Bechmann René Villadsen Ole William Petersen
author_facet	Lone Rønnov-Jessen Jiyoung Kim Nadine Goldhammer Marie Christine Klitgaard Martynas Smicius Marc Baker Bechmann René Villadsen Ole William Petersen
author_sort	Lone Rønnov-Jessen
title	Desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen
title_short	Desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen
title_full	Desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen
title_fullStr	Desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen
title_full_unstemmed	Desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen
title_sort	desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/9d1066b65c1f4879aa2a803d4e53a46b
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Desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen

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