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. Author manuscript; available in PMC: 2015 Feb 1.
Published in final edited form as: Semin Oncol. 2013 Dec 12;41(1):5–16. doi: 10.1053/j.seminoncol.2013.12.009

Figure 2. Proposed Model of Ligand-Independent PR Signaling in Lung Cancer.

Figure 2

Growth Factor (GF) ligands will induce Growth Factor Receptor (GFR) signaling, resulting in phosphorylation of PR at ser294 by the MAPK pathway, leading to both ligand-independent receptor activation and induction of proteosome-mediated PR degradation, and/or may lead to direct suppression of PR transcription by the Akt/mTor pathway (with a resultant decrease in PR protein expression). Such a pathway might explain why low PR in lung tumors was associated with worse survival, because it is indicative of high levels of GFR siginaling.