Heme-oxygenase-1 implications in cell morphology and the adhesive behavior of prostate cancer cells

• DOI: 10.18632/oncotarget.1826
• Publication Date: 2015-09-15T23:39:30Z
• Authors: Geraldine Gueron; Jimena Giudice; Pia Valacco; Alejandra Paez; Belen Elguero; Martin Toscani; Felipe Jaworski; Federico Coluccio...; Javier Cotignola; Marcelo Marti; Maria Binaghi; Nora Navone; Elba Vazquez
• Keywords: Adherens junction

// Geraldine Gueron 1 , Jimena Giudice 2 Pia Valacco 3  Alejandra Paez Belen Elguero , Martin Toscani Felipe Jaworski Federico Coluccio Leskow Javier Cotignola Marcelo Marti Maria Binaghi Nora Navone 4 Elba Vazquez Department of Biological Chemistry, School Sciences, University Buenos Aires, IQUIBICEN-CONICET, Intendente Guiraldes 2160, CABA Pathology and Immunology, Baylor College Medicine, One Plaza, Houston, TX, USA CEQUIBIEM-Department IQUIBICEN-CONICET Genitourinary Medical Oncology, The Texas, M. D. Anderson Cancer Center, Correspondence: Gueron, email: Vazquez, Keywords : Prostate Cancer, Heme-oxygenase-1, Muskelin, E-cadherin, B-catenin, Adherens Junctions, Received January 24, 2014 Accepted March 14, Published 16, Abstract cancer (PCa) is the second leading cause death in men. Although previous studies PCa have focused on cell adherens junctions (AJs), key players metastasis, they left molecular mechanisms unexplored. Inflammation involvement reactive oxygen species (ROS) are critical regulation adhesion integrity epithelium. Heme oxygenase-1 (HO-1) counteracts oxidative inflammatory damage. Here, we investigated whether HO-1 implicated adhesive morphological properties tumor cells. Genes differentially regulated by were enriched for motility biological processes. induction, increased E-cadherin β-catenin levels. Immunofluorescence analyses showed a striking remodeling E-cadherin/β-catenin based AJs under modulation. Interestingly, enhanced levels coincided with markedly change morphology. To further our analysis sought to identify binding proteins that might participate A proteomics approach identified as novel partner, strongly morphology regulation. These results define role modulating architecture cell-cell interactions, favoring less aggressive phenotype supporting its anti-tumoral function PCa.&nbsp