By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy
// Annalisa Petrelli 1,* , Rosachiara Carollo 2,* , Marilisa Cargnelutti 1 , Flora Iovino 2 , Maurizio Callari 3 , Daniela Cimino 4 , Matilde Todaro 2 , Laura Rosa Mangiapane 2 , Alessandro Giammona 2 , Adriana Cordova 2 , Filippo Montemurro 1 , Daniela Taverna 4 , Maria Grazia Daidone 3 , Giorgio Stassi 2,* and Silvia Giordano 1,* 1 University of Torino School of Medicine, Candiolo Cancer Institute-FPO, IRCCS, Str. Provinciale, Candiolo, Torino, Italy 2 Department of Surgical and Oncological Sciences, Cellular and Molecular Pathophysiology Laboratory, University of Palermo, Palermo, Italy 3 Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy 4 Molecular Biotechnology Center (MBC),…
Erratum: By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy
Basal-like breast cancer is an aggressive tumor subtype with a poor response to conventional therapies. Tumor formation and relapse are sustained by a cell subset of Breast Cancer Stem Cells (BrCSCs). Here we show that miR-100 inhibits maintenance and expansion of BrCSCs in basal-like cancer through Polo-like kinase1 (Plk1) down-regulation. Moreover, miR-100 favors BrCSC differentiation, converting a basal like phenotype into luminal. It induces the expression of a functional estrogen receptor (ER) and renders basal-like BrCSCs responsive to hormonal therapy. The key role played by miR-100 in breast cancer free-survival is confirmed by the analysis of a cohort of patients' tumors, which sho…
Stem Cell-Derived, microRNA-Carrying Extracellular Vesicles: A Novel Approach to Interfering with Mesangial Cell Collagen Production in a Hyperglycaemic Setting.
Extracellular vesicles (EVs) that are derived from stem cells are proving to be promising therapeutic options. We herein investigate the therapeutic potential of EVs that have been derived from different stem cell sources, bone-marrow (MSC) and human liver (HLSC), on mesangial cells (MCs) exposed to hyperglycaemia. By expressing a dominant negative STAT5 construct (ΔNSTAT5) in HG-cultured MCs, we have demonstrated that miR-21 expression is under the control of STAT5, which translates into Transforming Growth Factor beta (TGFβ) expression and collagen production. A number of approaches have been used to show that both MSC- and HLSC-derived EVs protect MCs from HG-induced damage via the trans…