User:ACCoogan/sandbox
Introduction
Epithelial–mesenchymal transition was first recognized as a feature of embryogenesis by Betty Hay in the 1980s.[1][2] EMT, and its reverse process, MET (mesenchymal-epithelial transition) are critical for development of many tissues and organs in the developing embryo, and numerous embryonic events such as gastrulation, neural crest formation, heart valve formation, palatogenesis and myogenesis.[3] Epithelial and mesenchymal cells differ in phenotype as well as function, though both share inherent plasticity.[2] Epithelial cells are closely connected to each other by tight junctions, gap junctions and adherens junctions, have an apico-basal polarity, polarization of the actin cytoskeleton and are bound by a basal lamina at their basal surface. Mesenchymal cells, on the other hand, lack this polarization, have a spindle-shaped morphology and interact with each other only through focal points.[4] Epithelial cells express high levels of E-cadherin, whereas mesenchymal cells express those of N-cadherin, fibronectin and vimentin. Thus, EMT entails profound morphological and phenotypic changes to a cell. Based on the biological context, EMT has been categorized into 3 types - developmental (Type I), fibrosis[5] and wound healing (Type II), and cancer (Type III).[6][7][8]
| Marker | Epithelial or Mesenchymal |
|---|---|
| E-cadherin | Epithelial |
| N-cadherin | Mesenchymal |
| Fibronectin | |
| Vimentin | |
| Transcription Factor | Epithelial or Mesenchymal |
| SNAI1/SNAI2 | Promotes mesenchymal |
| ZEB1/2 | |
| E47 | |
| ZLF8 | |
| Twist | |
| Goosecoid | |
| E2.2/TCF4 | |
| SIX1 | |
| FOXC2 | |
| GRHL2 | Promotes epithelial |
| ELF3/5 | |
| Signaling Pathway | Epithelial or Mesenchymal |
| TGF-β | Promotes mesenchymal |
| FGF | |
| HGF | |
| Wnt/β-catenin | |
| Notch | |
| Hypoxia | |
| Ras-MAPK | |
| Hedgehog |
In cancer progression and metastasis
Initiation of metastasis requires invasion, which is enabled by EMT.[9][10] Carcinoma cells in primary tumor lose cell-cell adhesion mediated by E-cadherin repression and break through the basement membrane with increased invasive properties, and enter the bloodstream through intravasation. Later, when these circulating tumor cells (CTCs) exit the bloodstream to form micro-metastases, they undergo MET for clonal outgrowth at these metastatic sites. Thus, EMT and MET form the initiation and completion of the invasion-metastasis cascade.[11] At this new metastatic site, the tumor may undergo other processes to optimize growth. For example, EMT has been associated with PD-L1 expression, particularly in lung cancer. Increased levels of PD-L1 suppresses the immune system which allows the cancer to spread more easily. [12]
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- ^ Kong D, Li Y, Wang Z, Sarkar FH (2011). "Cancer Stem Cells and Epithelial-to-Mesenchymal Transition (EMT)-Phenotypic Cells: Are They Cousins or Twins?". Cancers (Basel). 3 (1): 716–29. doi:10.3390/cancers30100716. PMC 3106306. PMID 21643534.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b Lamouille, Samy; Xu, Jian; Derynck, Rik (March 2014). "Molecular mechanisms of epithelial-mesenchymal transition". Nature Reviews. Molecular Cell Biology. 15 (3): 178–196. doi:10.1038/nrm3758. ISSN 1471-0080. PMC 4240281. PMID 24556840.
{{cite journal}}: CS1 maint: PMC format (link) - ^ Thiery JP, Acloque H, Huang YJ, Nieto MA (2009). "Epithelial-Mesenchymal Transitions in Development and Disease". Cell. 139 (5): 871–890. doi:10.1016/j.cell.2009.11.007.
- ^ Thiery JP, Sleeman JP (2006). "Complex networks orchestrate epithelial-mesenchymal transitions". Nature Reviews Molecular Cell Biology. 7: 131–142. doi:10.1038/nrm1835.
- ^ Phua, YL; Martel, N; Pennisi, DJ; Little, MH; Wilkinson, L (April 2013). "Distinct sites of renal fibrosis in Crim1 mutant mice arise from multiple cellular origins". The Journal of pathology. 229 (5): 685–96. doi:10.1002/path.4155. PMID 23224993.
- ^ Kalluri R, Weinberg RA (2009). "The basics of epithelial-mesenchymal transition". Journal of Clinical Investigation. 119 (6): 1420–1428. doi:10.1172/JCI39104. PMC 2689101. PMID 19487818.
- ^ Sciacovelli, Marco; Frezza, Christian (2017-04-26). "Metabolic reprogramming and epithelial-to-mesenchymal transition in cancer". The FEBS journal. doi:10.1111/febs.14090. ISSN 1742-4658. PMID 28444969.
- ^ Li, Linna; Li, Wenliang (June 2015). "Epithelial-mesenchymal transition in human cancer: comprehensive reprogramming of metabolism, epigenetics, and differentiation". Pharmacology & Therapeutics. 150: 33–46. doi:10.1016/j.pharmthera.2015.01.004. ISSN 1879-016X. PMID 25595324.
- ^ Hanahan, D.; Weinberg, R. A. (2000-01-07). "The hallmarks of cancer". Cell. 100 (1): 57–70. ISSN 0092-8674. PMID 10647931.
- ^ Hanahan, Douglas; Weinberg, Robert A. (2011-03-04). "Hallmarks of cancer: the next generation". Cell. 144 (5): 646–674. doi:10.1016/j.cell.2011.02.013. ISSN 1097-4172. PMID 21376230.
- ^ Chaffer CL, Weinberg RA (2011). "A perspective on cancer cell metastasis". Science. 331 (6024): 1559–1564. doi:10.1126/science.1203543. PMID 21436443.
- ^ Ye, Xin; Weinberg, Robert A. (2015-11). "Epithelial-Mesenchymal Plasticity: A central regulator of cancer progression". Trends in cell biology. 25 (11): 675–686. doi:10.1016/j.tcb.2015.07.012. ISSN 0962-8924. PMC 4628843. PMID 26437589.
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