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. 2021 Apr 28;11(5):564. doi: 10.3390/brainsci11050564

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The molecular mechanism proposed for the activation or inhibition of EMT by E2 and TGF-β effects in human GBM cells. E2 and TGF-β promote EMT through ER and Smad, respectively. Crosstalk between ER and Smad inhibits EMT promoted independently by E2 and TGF-β. It is unknown whether the inhibition between E2 and TGF-β is through a direct or indirect interaction between ER and Smads. Epithelial–mesenchymal transition (EMT); 17β-estradiol (E2), estrogen receptor (ER); glioblastoma (GBM); transforming growth factor β (TGF-β); type I/II serine/threonine kinase receptor (TβRI/II).