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. 2014 Mar 21;13:69. doi: 10.1186/1476-4598-13-69

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Copyright © 2014 Nuvoli et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Hypothesized mechanism of action of exemestane on MPM cells. The GPCR receptor binds estrogen and cause estrogen-mediated cAMP stimulation and PI3K cascade. PI3K phosphorylates AKT (pAkt) which in turn regulates Bcl-xL, anti-apoptotic protein. cAMP stimulates PKA, which in turn activates CREB that translocates into the nucleus and acts as a transcription factor for CD44. The action of exemestane is carried out by reducing the levels of estradiol, its binding with GPCR and related downstream pathway.