Contemporary changes and civil society in Portugal and the Russian Federation

Portugal and the Russian Federation share some aspects of traditional culture and similar experiences in modern history, but they also exhibit significant differences that determine specific modes of civil society’s development. Results of a comparative and diachronic analysis show that the major differences between the two countries reside in civil society’s openness and composition. Organized civil society is not very distinct in relative size when comparing Portugal and the Russian Federation, but it is globally more autonomous, expressive, trusted and institutionalized in Portugal than in the Russian Federation and among the factors that contribute to this condition are an earlier and revolutionary transition to democracy, a larger middle class, a greater prevalence of the value of interdependence, and a regime that endorses bigger public social expenditure in Portugal, all this within the framework of the European Union that has a longer history of social demand and institutional incentives for civil society. Despite those unequal conditions, civil society faces similar current challenges in both countries, mainly with the outsourcing of the public provision of social services.info:eu-repo/semantics/acceptedVersio

The splicing factor SRSF1 regulates apoptosis and proliferation to promote mammary epithelial cell transformation

The splicing-factor oncoprotein SRSF1 (also known as SF2/ASF or ASF/SF2) is upregulated in breast cancers. We investigated the ability of SRSF1 to transform human and mouse mammary epithelial cells in vivo and in vitro. SRSF1-overexpressing COMMA-1D cells formed tumors, following orthotopic transplantation to reconstitute the mammary gland. In three-dimensional (3D) culture, SRSF1-overexpressing MCF-10A cells formed larger acini than control cells, reflecting increased proliferation and delayed apoptosis during acinar morphogenesis. These effects required the first RNA-recognition motif and nuclear functions of SRSF1. SRSF1 overexpression promoted alternative splicing of BIM (also known as BCL2L11) and BIN1 to produce isoforms that lack pro-apoptotic functions and contribute to the phenotype. Finally, SRSF1 cooperated specifically with MYC to transform mammary epithelial cells, in part by potentiating eIF4E activation, and these cooperating oncogenes are significantly coexpressed in human breast tumors. Thus, SRSF1 can promote breast cancer, and SRSF1 itself or its downstream effectors may be valuable targets for the development of therapeutics