Snail1 expression is required for sarcomagenesis

Under a Creative Commons license.-- et al.Snail1 transcriptional repressor is a major inducer of epithelial-to mesenchymal transition but is very limitedly expressed in adult animals. We have previously demonstrated that Snail1 is required for the maintenance of mesenchymal stem cells (MSCs), preventing their premature differentiation. Now, we show that Snail1 controls the tumorigenic properties of mesenchymal cells. Increased Snail1 expression provides tumorigenic capabilities to fibroblastic cells; on the contrary, Snail1 depletion decreases tumor growth. Genetic depletion of Snail1 in MSCs that are deficient in p53 tumor suppressor downregulates MSC markers and prevents the capability of these cells to originate sarcomas in immunodeficient SCID mice. Notably, an analysis of human sarcomas shows that, contrarily to epithelial tumors, these neoplasms display high Snail1 expression. This is particularly clear for undifferentiated tumors, 9which are associated with poor outcome. Together, our results indicate a role for Snail1 in the generation of sarcomas.This study was funded by grants awarded by la Fundación Científica de la Asociación Española contra el Cáncer (to A.G.H., J.I.C., and F.B.), Fundación Sandra Ibarra and Ministerio de Ciencia y Tecnología (SAF2010-16089) to A.G.H. and also by RD12/0036/0005, part of “Plan Nacional de I+D+I” and cofunded by “Instituto de Salud Carlos III (ISCIII)-Subdirección General de Evaluación and Fondo Europeo de Desarrollo Regional (FEDER)”. We also acknowledge support from Fundació La Marató de TV3 (120130), to A.G.H., ISCIII/FEDER (RD12/0036/041, RD12/0036/051, and RD12/0036/021), Generalitat de Catalunya (2009SGR867 and 2009SGR321; Xarxa de Bancs de Tumors), CAM (CAM S2010-BMD2344-Colomics2), and Fundació Cellex (Barcelona). R.B. and L.A.-C. were recipients from “Formación de Personal Investigador” predoctoral fellowships.Peer reviewe

EMT-independent Snail1 modulation of tumor invasion

40 p.-6 fig.Snail1 transcriptional factor is essential for triggering epithelial-to-mesenchymal transition (EMT) and inducing tumor cell invasion. We report here an additional, EMTindependent action of Snail1 on tumor invasion: its expression in cancer-associated fibroblasts is necessary for enhancement by these cells on epithelial cells tumor invasion. Snail1 expression in fibroblast requires signals derived from tumor cells such as TGF-; reciprocally, in fibroblasts Snail1 organizes a complex program that favors collective invasion of epithelial cells at least in part by the secretion of diffusible signaling molecules, such as prostaglandin E2. The capability of human or murine tumor-derived cancer associated fibroblasts to promote tumor invasion is associated to Snail1 expression and obliterated by Snail1 depletion. In vivo experiments show that Snail1 depletion in mice prevents the invasion of breast tumors and epithelial tumor cells co-xenografted with Snail1-depleted fibroblasts originate tumors with lower invasion than those transplanted with control fibroblasts. Therefore, these results demonstrate that the role of Snail1 in tumor invasion is not limited to EMT but dependent on its expression in stromal fibroblasts where it orchestrates its activation and the crosstalk with epithelial tumor cells. Moreover, they point to the interference of Snail expression as a promising target for preventing the action of stromal fibroblasts on tumor progression.This work was funded by grants from Fundación Científica de la Asociación Española contra el Cáncer to AGH, JIC and FB, and Ministerio de Economía(SAF2013-48849-C2-1-R) and Fundació La Marató de TV3 (120130) to AGH. We also thank the support from Instituto Carlos III (RD12/0036/005 and RD12/0036/004,1 part of the Plan Nacional I+D+I and cofounded by the ISCIII-Subdirección General de Evaluación and Fondo Europeo de Desarrollo Regional-FEDER) and Generalitat de Catalunya (2014 SGR 32).Peer reviewe

Tailoring the ORR and HER electrocatalytic performances of gold nanoparticles through metal-ligand interfaces

The oxygen reduction (ORR) and hydrogen evolution (HER) reactions are the most important cathodic processes involved in fuel cell and water splitting technologies, respectively. The development of bifunctional electrocatalyst materials plays a key role in the rapid advancement of these hydrogen-based renewable energy strategies. This work proposes citrate-stabilized gold nanoparticles (AuNPs) as a bifunctional electrocatalyst for ORR and HER. The capping ligand has a great influence on their resulting electrocatalytic performance. A simple ligand exchange method based on concentration gradients has been optimized. The surface structure of the different ligand-stabilized AuNPs was inferred by lead underpotential deposition (Pb-UPD). Static and dynamic electrochemical studies for both ORR and HER have been performed using different ligand-stabilized AuNPs as electrocatalysts, demonstrating that the citrate ligand confers the best performance. This work suggests that non-doped chemically synthesized AuNPs may be suitable as a bifunctional electrocatalyst in fuel cells and hydrogen production. © The Royal Society of Chemistry 2019

Correction: Tailoring the ORR and HER electrocatalytic performances of gold nanoparticles through metal-ligand interfaces (Journal of Materials Chemistry A (2019) DOI: 10.1039/c9ta05492h)

The authors regret the following minor errors in the published article. In eqn (4), a minus sign was missing from the ?nal exponential term. The correct version of eqn (4) is as follows: (Equetion Persented). © The Royal Society of Chemistry 201