EMT and tumor metastasis
By S. Heerboth, Genevieve Housman, M. Leary, Mckenna Longacre, Shannon Byler, K. Lapinska, A. Willbanks, S. Sarkar. Clinical and Translational Medicine, 2015
716 citations recorded by the source corpus.
EMT and MET comprise the processes by which cells transit between epithelial and mesenchymal states, and they play integral roles in both normal development and cancer metastasis. This article reviews these processes and the molecular pathways that contribute to them. First, we compare embryogenesis and development with cancer metastasis. We then discuss the signaling pathways and the differential expression and down-regulation of receptors in both tumor cells and stromal cells, which play a role in EMT and metastasis. We further delve into the clinical implications of EMT and MET in several types of tumors, and lastly, we discuss the role of epigenetic events that regulate EMT/MET processes. We hypothesize that reversible epigenetic events regulate both EMT and MET, and thus, also regulate the development of different types of metastatic cancers.
Subfields: Genetics, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/f9906dd0d6431728be5cfe20601027a66be50b9f
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
Citations in the corpus
- Natural Killer Cells: Development, Maturation, and Clinical Utilization (2018, background): “Genomic mutations that arise during the transformation process are reflected by a variety of phenotypic changes which alter the expression of cell surface molecules, including downregulation of the inhibitory “self” MHC-I (200, 249).”