Cancers, Vol. 15, Pages 2317: Myo-Inositol Reverses TGF- & beta;1-Induced EMT in MCF-10A Non-Tumorigenic Breast Cells

Cancers, Vol. 15, Pages 2317: Myo-Inositol Reverses TGF-β1-Induced EMT in MCF-10A Non-Tumorigenic Breast Cells Cancers doi: 10.3390/cancers15082317 Authors: Noemi Monti Simona Dinicola Alessandro Querqui Gianmarco Fabrizi Valeria Fedeli Luisa Gesualdi Angela Catizone Vittorio Unfer Mariano Bizzarri Epithelial-Mesenchymal Transition (EMT), triggered by external and internal cues in several physiological and pathological conditions, elicits the transformation of epithelial cells into a mesenchymal-like phenotype. During EMT, epithelial cells lose cell-to-cell contact and acquire unusual motility/invasive capabilities. The associated architectural and functional changes destabilize the epithelial layer consistency, allowing cells to migrate and invade the surrounding tissues. EMT is a critical step in the progression of inflammation and cancer, often sustained by a main driving factor as the transforming growth factor-β1 (TGF-β1). Antagonizing EMT has recently gained momentum as an attractive issue in cancer treatment and metastasis prevention. Herein, we demonstrate the capability of myo-inositol (myo-Ins) to revert the EMT process induced by TGF-β1 on MCF-10A breast cells. Upon TGF-β1 addition, cells underwent a dramatic phenotypic transformation, as witnessed by structural (disappearance of the E-cadherin–β-catenin complexes and the emergence of a mesenchymal shape)...
Source: Cancers - Category: Cancer & Oncology Authors: Tags: Article Source Type: research