English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

At its core, epithelial-mesenchymal transition (EMT) programs are well-established physiological processes that transpire during embryogenesis to facilitate the development of the mesoderm and neural crest, and during adulthood to oversee the repair of wounded tissues (1-3). Epithelial cells undergoing EMT programs downregulate epithelial markers (e.g., E-cadherin) and upregulate mesenchymal markers (e.g., vimentin), leading to stark changes in cell morphology and behavior. For instance, epithelial cells are typically arranged as a single layer of polarized cells that exhibit strong cell-cell contacts, a phenotype that gives way during EMT programs to the generation of apolar mesenchymal-like cells that exhibit elongated spindle morphologies (1-3). Importantly, the phenomenon of EMT can be hijacked by pathological processes, including fibrosis, inflammatory conditions, and the progression and metastasis of solid tumors (1).

The propensity for epithelial-mesenchymal transitions is dictated by chromatin states in the cancer cell of origin