Mohit Kumar Jolly

TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.

TL;DR: The operating principles of the core regulatory network for EMT/MET that acts as a “three-way” switch giving rise to three distinct phenotypes – E, M and hybrid E/M are reviewed and a theoretical framework that can elucidate the role of many other players in regulating epithelial plasticity is presented.

TL;DR: A unique model of the microRNA (miR)-based coupled chimeric modules underlying this core circuit is devised, showing that the miR-200/ZEB module functions as a ternary switch, allowing not only for the epithelial and mesenchymal phenotypes but also for a hybrid phenotype with mixed characteristics of collective cell migration, as seen in branching morphogenesis and wound closure.

TL;DR: Based on recent literature, indicating a co-expression of epithelial and mesenchymal markers in many tumor buds, it is posited that tumor budding is a manifestation of this hybrid epithelial/mesenchyal phenotype displaying collective cell migration.

TL;DR: The results suggest that partial EMT, i.e. a hybrid E/M phenotype, need not be ‘metastable’, and strengthen the emerging notion that partialEMT, but not necessarily a complete E MT, is associated with aggressive tumor progression.