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Int. J. Mol. Sci. 2019, 20(8), 1815;

STAT3 Post-Translational Modifications Drive Cellular Signaling Pathways in Prostate Cancer Cells

Department of Biochemical Sciences “A. Rossi Fanelli” and Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University, P.le A. Moro 5, 00185 Rome, Italy
Department of Biological Regulation, Weizmann Institute of Science, 234 Herzl Street, 7610001 Rehovot, Israel
Department of Gynecological-Obstretic Science and Urologic Sciences, Sapienza University, V.le Dell’Università, 00185 Rome, Italy
Department of Research, Advanced Diagnostics, and Technological Innovation, Translational Research Area, Regina Elena National Cancer Institute; via Elio Chianesi, 53, 00144 Rome, Italy
Author to whom correspondence should be addressed.
Received: 5 March 2019 / Revised: 8 April 2019 / Accepted: 9 April 2019 / Published: 12 April 2019
PDF [3224 KB, uploaded 12 April 2019]


STAT3 is an oncoprotein overexpressed in different types of tumors, including prostate cancer (PCa), and its activity is modulated by a variety of post-translational modifications (PTMs). Prostate cancer represents the most common cancer diagnosed in men, and each phase of tumor progression displays specific cellular conditions: inflammation is predominant in tumor’s early stage, whereas oxidative stress is typical of clinically advanced PCa. The aim of this research is to assess the correspondence between the stimulus-specificity of STAT3 PTMs and definite STAT3-mediated transcriptional programs, in order to identify new suitable pharmacological targets for PCa treatment. Experiments were performed on less-aggressive LNCaP and more aggressive DU-145 cell lines, simulating inflammatory and oxidative-stress conditions. Cellular studies confirmed pY705-STAT3 as common denominator of all STAT3-mediated signaling. In addition, acK685-STAT3 was found in response to IL-6, whereas glutC328/542-STAT3 and pS727-STAT3 occurred upon tert-butyl hydroperoxyde (tBHP) treatment. Obtained results also provided evidence of an interplay between STAT3 PTMs and specific protein interactors such as P300 and APE1/Ref-1. In accordance with these outcomes, mRNA levels of STAT3-target genes seemed to follow the differing STAT3 PTMs. These results highlighted the role of STAT3 and its PTMs as drivers in the progression of PCa. View Full-Text
Keywords: STAT3; post translational modification; prostate cancer; transduction signaling STAT3; post translational modification; prostate cancer; transduction signaling

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Cocchiola, R.; Rubini, E.; Altieri, F.; Chichiarelli, S.; Paglia, G.; Romaniello, D.; Carissimi, S.; Giorgi, A.; Giamogante, F.; Macone, A.; Perugia, G.; Gurtner, A.; Eufemi, M. STAT3 Post-Translational Modifications Drive Cellular Signaling Pathways in Prostate Cancer Cells. Int. J. Mol. Sci. 2019, 20, 1815.

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