Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis.
By Jing Yang, R. Weinberg. Developmental Cell, 2008
3,104 citations recorded by the source corpus.
The epithelial-mesenchymal transition is a highly conserved cellular program that allows polarized, immotile epithelial cells to convert to motile mesenchymal cells. This important process was initially recognized during several critical stages of embryonic development and has more recently been implicated in promoting carcinoma invasion and metastasis. In this review, we summarize and compare major signaling pathways that regulate the epithelial-mesenchymal transitions during both development and tumor metastasis. Studies in both fields are critical for our molecular understanding of cell migration and morphogenesis.
Subfields: Cell Biology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/e9983bd721c945ca6f97a15214b21d0d2da55eae
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Citations in the corpus
- CD44: can a cancer-initiating cell profit from an abundantly expressed molecule? (2011, background): “Stem cells, adhesion, homing and migration Shared features between CICs and stem cells are frequently linked to secondary events such as interaction with a niche, the process of epithelial–mesenchymal transition (EMT)”
- Tumors as organs: complex tissues that interface with the entire organism (2010, neutral): “…of E-cadherin, b-catenin is released from the cell membrane and translocates to the nucleus, where it activates the transcription factor lymphoid enhancer factor/T-cell factor (LEF/ TCF) and induces the expression of target genes that promote motility and inhibit adhesion (Yang and Weinberg, 2008).”
- Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “Snail2 also has a well-established role in the induction of EMT during cancer metastasis and is involved in gastrulation and the development and migration of the neural crest (17, 33).”
- Cadherins and cancer: how does cadherin dysfunction promote tumor progression? (2008, background): “kidney) cells: polarity of an apical protein is independent of tight junctions while segregation of a basolateral marker requires cell–cell interactions. J Cell Biol 104: 905–916. Vleminckx K, Vakaet L, Mareel M, Fiers W, Van Roy F. (1991). Genetic manipulation of E-cadherin expression by epithelial”
- MET signalling: principles and functions in development, organ regeneration and cancer (2010, background): “This resemblance is not simply a biological correlate, it has a common mechanistic basis: cancer cells resurrect the latent schemes of cellular reorganization, which are usually confined to embryonic development and damaged adult organs, and leverage them to become competent for metastasizatio”