17-Estradiol Activates HSF1 via MAPK Signaling in ER-Positive Breast Cancer Cells.

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ID: 64009
2019
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Abstract
Heat Shock Factor 1 (HSF1) is a key regulator of gene expression during acute environmental stress that enables the cell survival, which is also involved in different cancer-related processes. A high level of HSF1 in estrogen receptor (ER)-positive breast cancer patients correlated with a worse prognosis. Here we demonstrated that 17-estradiol (E2), as well as xenoestrogen bisphenol A and ER agonist propyl pyrazole triol, led to HSF1 phosphorylation on S326 in ER positive but not in ER-negative mammary breast cancer cells. Furthermore, we showed that MAPK signaling (via MEK1/2) but not mTOR signaling was involved in E2/ER-dependent activation of HSF1. E2-activated HSF1 was transcriptionally potent and several genes essential for breast cancer cells growth and/or ER action, including , , , , and , were activated by E2 in a HSF1-dependent manner. Our findings suggest a hypothetical positive feedback loop between E2/ER and HSF1 signaling, which may support the growth of estrogen-dependent tumors.
Reference Key
vydra201917estradiolcancers Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Vydra, Natalia;Janus, Patryk;Toma-Jonik, Agnieszka;Stokowy, Tomasz;Mrowiec, Katarzyna;Korfanty, Joanna;Długajczyk, Anna;Wojtaś, Bartosz;Gielniewski, Bartłomiej;Widłak, Wiesława;
Journal Cancers
Year 2019
DOI
E1533
URL
Keywords
bisphenol a estrogen heat shock factor 1 mek1/2 xenoestrogen nanoparticles water quality amalgam nanoplates spectral blue shift

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