Relevant bibliographies by topics / Epithelial mesenchyme transition

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Epithelial mesenchyme transition'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Epithelial mesenchyme transition"

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Sheng, Wang, Guizhi Wang, David P. La Pierre, Jianping Wen, Zhaoqun Deng, Chung-Kwun Amy Wong, Daniel Y. Lee, and Burton B. Yang. "Versican Mediates Mesenchymal-Epithelial Transition." Molecular Biology of the Cell 17, no. 4 (April 2006): 2009–20. http://dx.doi.org/10.1091/mbc.e05-10-0951.

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Versican is a large extracellular chondroitin sulfate proteoglycan that belongs to the family of lecticans. Alternative splicing of versican generates at least four isoforms named V0, V1, V2, and V3. We show here that ectopic expression of versican V1 isoform induced mesenchymal-epithelial transition (MET) in NIH3T3 fibroblasts, and inhibition of endogenous versican expression abolished the MET in metanephric mesenchyme. MET in NIH3T3 cells was demonstrated by morphological changes and dramatic alterations in both membrane and cytoskeleton architecture. Molecular analysis showed that V1 promoted a “switch” in cadherin expression from N- to E-cadherin, resulting in epithelial specific adhesion junctions. V1 expression reduced vimentin levels and induced expression of occludin, an epithelial-specific marker, resulting in polarization of V1-transfected cells. Furthermore, an MSP (methylation-specific PCR) assay showed that N-cadherin expression was suppressed through methylation of its DNA promoter. Exogenous expression of N-cadherin in V1-transfected cells reversed V1's effect on cell aggregation. Reduction of E-cadherin expression by Snail transfection and siRNA targeting E-cadherin abolished V1-induced morphological alteration. Transfection of an siRNA construct targeting versican also reversed the changed morphology induced by V1 expression. Silencing of endogenous versican prevented MET of metanephric mesenchyme. Taken together, our results demonstrate the involvement of versican in MET: expression of versican is sufficient to induce MET in NIH3T3 fibroblasts and reduction of versican expression decreased MET in metanephric mesenchyme.
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Li, J., J. Xu, Y. Cui, L. Wang, B. Wang, Q. Wang, X. Zhang, M. Qiu, and Z. Zhang. "Mesenchymal Sufu Regulates Development of Mandibular Molars via Shh Signaling." Journal of Dental Research 98, no. 12 (September 9, 2019): 1348–56. http://dx.doi.org/10.1177/0022034519872679.

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Sonic hedgehog ( Shh) in dental epithelium regulates tooth morphogenesis by epithelial-mesenchymal signaling transduction. However, the action of Shh signaling regulation in this process is not well understood. Here we find that mesenchymal Suppressor of Fused ( Sufu), a major negative regulator of Shh signaling, plays an important role in modulating the tooth germ morphogenesis during the bud-to-cap stage transition. Deletion of Sufu in dental mesenchyme by Dermo1-Cre mice leads to delayed development of mandibular molar into cap stage with defect of primary enamel knot (EK) formation. We show the disruption of cell proliferation and programmed cell death in dental epithelium and mesenchyme in Sufu mutants. Epithelial-specific adhesion molecule E-cadherin is evidently reduced in the bilateral basal cells of tooth germ at E14.5. The cells in the presumptive EK, predominantly expressing P-cadherin, appear stratified but fail to condense. Moreover, the transcripts of primary EK marker genes, including Shh, Fgf4, and p21, are significantly decreased compared to controls. In contrast, we find that deficiency of Sufu results in elevation of Shh signaling in mesenchyme, indicated by the significant upregulation of Gli1 and Ptch1. Meanwhile, the expression of Bmp4 and Fgf3, the critical factors of mesenchymal-epithelial induction, is significantly inhibited in dental mesenchyme. Furthermore, the expression of Runx2 experiences a transient decrease at the bud stage. Taken together, these data suggest that mesenchymal Sufu is necessary for tuning the Shh signaling, which may act as an upstream modulator of Bmp4 and Fgf3 to coordinate the interplay between the dental mesenchyme and epithelium of tooth germ.
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Huber, Stephan M., Gerald S. Braun, Stephan Segerer, Rüdiger W. Veh, and Michael F. Horster. "Metanephrogenic mesenchyme-to-epithelium transition induces profound expression changes of ion channels." American Journal of Physiology-Renal Physiology 279, no. 1 (July 1, 2000): F65—F76. http://dx.doi.org/10.1152/ajprenal.2000.279.1.f65.

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The expression patterns of plasma membrane transporters that specify the epithelial cell type are acquired with ontogeny. To study this process during metanephrogenic mesenchyme-to-epithelium transition, branching ureteric buds with their adjacent mesenchymal blastema (mouse embryonic day E14) were dissected and explanted on a collagen matrix. In culture, induced mesenchymal cells condensed, aggregated, and converted to the comma- and S-shaped body. During in vitro condensation and aggregation, transcription factor Pax-2 protein was downregulated while the epithelial markers E-cadherin and β-catenin proteins were upregulated. In addition, Wilms' tumor suppressor protein WT-1 was detectable upon condensation and downregulated in the S stage, where expression persisted in the long arm of the S. Patch-clamp, whole cell conductance ( G, in nS/10 pF) of pre-epithelial condensed mesenchymal cells ( n = 7) was compared with that of tubular proximal S-shaped-body epithelium ( n = 6). Both stages expressed E-cadherin and WT-1 mRNA, as demonstrated by single-cell RT-PCR, testifying further to the epithelial as well as the nephrogenic commitment of the recorded cells. Mesenchymal cells exhibited whole cell currents ( G = 6.7 ± 1.3) with reversal potentials ( V rev, in mV) near equilibrium potential for Cl− ( E Cl) ( V rev = −40 ± 7) suggestive of a high fractional Cl− conductance. Currents of the S-shaped-body cells ( G = 4.0 ± 1.1), in sharp contrast, had a V rev at E K ( V rev = −82 ± 6) indicating a high fractional K+ conductance. Further, analysis of K+-selective whole cell tail currents and single-channel recording revealed a change in K+ channel expression. Also, Kir6.1 K+ channel mRNA and protein were downregulated between both stages, whereas KvLQT K+ channel mRNA was abundant throughout. In conclusion, metanephrogenic mesenchyme-to-epithelium transition is accompanied by a profound reorganization of plasma membrane ion channel conductance.
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Kanwar, Yashpal S., Jun Wada, Sun Lin, Farhad R. Danesh, Sumant S. Chugh, Qiwei Yang, Tushar Banerjee, and Jon W. Lomasney. "Update of extracellular matrix, its receptors, and cell adhesion molecules in mammalian nephrogenesis." American Journal of Physiology-Renal Physiology 286, no. 2 (February 2004): F202—F215. http://dx.doi.org/10.1152/ajprenal.00157.2003.

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One of the hallmarks of mammalian nephrogenesis includes a mesenchymal-epithelial transition that is accomplished by intercalation of the ureteric bud, an epithelium-lined tubelike structure, into an undifferentiated mesenchyme, and the latter then undergoes an inductive transformation and differentiates into an epithelial phenotype. At the same time, the differentiating mesenchyme reciprocates by inducing branching morphogenesis of the ureteric bud, which forms a treelike structure with dichotomous iterations. These reciprocal inductive interactions lead to the development of a functioning nephron unit made up of a glomerulus and proximal and distal tubules. The inductive interactions and differentiation events are modulated by a number of transcription factors, protooncogenes, and growth factors and their receptors, which regulate the expression of target morphogenetic modulators including the ECM, integrin receptors, and cell adhesion molecules. These target macromolecules exhibit spatiotemporal and stage-specific developmental regulation in the metanephros. The ECM molecules expressed at the epithelial-mesenchymal interface are perhaps the most relevant and conducive to the paracrine-juxtacrine interactions in a scenario where the ligand is expressed in the mesenchyme while the receptor is located in the ureteric bud epithelium or vice versa. In addition, expression of the target ECM macromolecules is regulated by matrix metalloproteinases and their inhibitors to generate a concentration gradient at the interface to further propel epithelial-mesenchymal interactions so that nephrogenesis can proceed seamlessly. In this review, we discuss and update our current understanding of the role of the ECM and related macromolecules with respect to metanephric development.
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Piras, Monica, Clara Gerosa, Terenzio Congiu, Flaviana Cau, Daniela Fanni, Giuseppina Pichiri, Pierpaolo Coni, et al. "Toward the renal vesicle: Ultrastructural investigation of the cap mesenchyme splitting process in the developing kidney." Journal of Public Health Research 11, no. 4 (October 2022): 227990362211240. http://dx.doi.org/10.1177/22799036221124076.

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Background: A complex sequence of morphogenetic events leads to the development of the adult mouse kidney. In the present study, we investigated the morphological events that characterize the early stages of the mesenchymal-to-epithelial transition of cap mesenchymal cells, analyzing in depth the relationship between cap mesenchymal induction and ureteric bud (UB) branching. Design and methods: Normal kidneys of newborn non-obese diabetic (NOD) mice were excised and prepared for light and electron microscopic examination. Results: Nephrogenesis was evident in the outer portion of the renal cortex of all examined samples. This process was mainly due to the interaction of two primordial derivatives, the ureteric bud and the metanephric mesenchyme. Early renal developmental stages were initially characterized by the formation of a continuous layer of condensed mesenchymal cells around the tips of the ureteric buds. These caps of mesenchymal cells affected the epithelial cells of the underlying ureteric bud, possibly inducing their growth and branching. Conclusions: The present study provides morphological evidence of the reciprocal induction between the ureteric bud and the metanephric mesenchyme showing that the ureteric buds convert mesenchyme to epithelium that in turn stimulates the growth and the branching of the ureteric bud.
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Liu, Yang, Yu Fang, Lili Bao, Feng Wu, Shilong Wang, and Siyu Hao. "Intercellular Communication Reveals Therapeutic Potential of Epithelial-Mesenchymal Transition in Triple-Negative Breast Cancer." Biomolecules 12, no. 10 (October 14, 2022): 1478. http://dx.doi.org/10.3390/biom12101478.

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(1) Background: Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with high intra-tumoral heterogeneity. The epithelial-mesenchymal transition (EMT) is one of the inducers of cancer metastasis and migration. However, the description of the EMT process in TNBC using single-cell RNA sequencing (scRNA-seq) remains unclear. (2) Methods: In this study, we analyzed 8938 cellular gene expression profiles from five TNBC patients. We first scored each malignant cell based on functional pathways to determine its EMT characteristics. Then, a pseudo-time trajectory analysis was employed to characterize the cell trajectories. Furthermore, CellChat was used to identify the cellular communications. (3) Results: We identified 888 epithelium-like and 846 mesenchyme-like malignant cells, respectively. A further pseudo-time trajectory analysis indicated the transition trends from epithelium-like to mesenchyme-like in malignant cells. To characterize the potential regulators of the EMT process, we identified 10 dysregulated transcription factors (TFs) between epithelium-like and mesenchyme-like malignant cells, in which overexpressed forkhead box protein A1 (FOXA1) was recognized as a poor prognosis marker of TNBC. Furthermore, we dissected the cell-cell communications via ligand-receptor (L-R) interactions. We observed that tumor-associated macrophages (TAMs) may support the invasion of malignant epithelial cells, based on CXCL-CXCR2 signaling. The tumor necrosis factor (TNF) signaling pathway secreted by TAMs was identified as an outgoing communication pattern, mediating the communications between monocytes/TAMs and malignant epithelial cells. Alternatively, the TNF-related ligand-receptor (L-R) pairs showed promising clinical implications. Some immunotherapy and anti-neoplastic drugs could interact with the L-R pairs as a potential strategy for the treatment of TNBC. In summary, this study enhances the understanding of the EMT process in the TNBC microenvironment, and dissections of EMT-related cell communications also provided us with potential treatment targets.
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Wineberg, Yishay, Tali Hana Bar-Lev, Anna Futorian, Nissim Ben-Haim, Leah Armon, Debby Ickowicz, Sarit Oriel, et al. "Single-Cell RNA Sequencing Reveals mRNA Splice Isoform Switching during Kidney Development." Journal of the American Society of Nephrology 31, no. 10 (July 10, 2020): 2278–91. http://dx.doi.org/10.1681/asn.2019080770.

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BackgroundDuring mammalian kidney development, nephron progenitors undergo a mesenchymal-to-epithelial transition and eventually differentiate into the various tubular segments of the nephron. Recently, Drop-seq single-cell RNA sequencing technology for measuring gene expression from thousands of individual cells identified the different cell types in the developing kidney. However, that analysis did not include the additional layer of heterogeneity that alternative mRNA splicing creates.MethodsFull transcript length single-cell RNA sequencing characterized the transcriptomes of 544 individual cells from mouse embryonic kidneys.ResultsGene expression levels measured with full transcript length single-cell RNA sequencing identified each cell type. Further analysis comprehensively characterized splice isoform switching during the transition between mesenchymal and epithelial cellular states, which is a key transitional process in kidney development. The study also identified several putative splicing regulators, including the genes Esrp1/2 and Rbfox1/2.ConclusionsDiscovery of the sets of genes that are alternatively spliced as the fetal kidney mesenchyme differentiates into tubular epithelium will improve our understanding of the molecular mechanisms that drive kidney development.
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Igietseme, Joseph U., Yusuf Omosun, Olga Stuchlik, Matthew S. Reed, James Partin, Qing He, Kahaliah Joseph, et al. "Role of Epithelial-Mesenchyme Transition in Chlamydia Pathogenesis." PLOS ONE 10, no. 12 (December 17, 2015): e0145198. http://dx.doi.org/10.1371/journal.pone.0145198.

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Mouneimne, Ghassan, and Joan S. Brugge. "YB-1 Translational Control of Epithelial-Mesenchyme Transition." Cancer Cell 15, no. 5 (May 2009): 357–59. http://dx.doi.org/10.1016/j.ccr.2009.04.006.

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Francou, Alexandre, and Kathryn V. Anderson. "The Epithelial-to-Mesenchymal Transition in Development and Cancer." Annual Review of Cancer Biology 4, no. 1 (March 9, 2020): 197–220. http://dx.doi.org/10.1146/annurev-cancerbio-030518-055425.

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Epithelial-to-mesenchymal transitions (EMTs) are complex cellular processes where cells undergo dramatic changes in signaling, transcriptional programming, and cell shape, while directing the exit of cells from the epithelium and promoting migratory properties of the resulting mesenchyme. EMTs are essential for morphogenesis during development and are also a critical step in cancer progression and metastasis formation. Here we provide an overview of the molecular regulation of the EMT process during embryo development, focusing on chick and mouse gastrulation and neural crest development. We go on to describe how EMT regulators participate in the progression of pancreatic and breast cancer in mouse models, and discuss the parallels with developmental EMTs and how these help to understand cancer EMTs. We also highlight the differences between EMTs in tumor and in development to arrive at a broader view of cancer EMT. We conclude by discussing how further advances in the field will rely on in vivo dynamic imaging of the cellular events of EMT.
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Dissertations / Theses on the topic "Epithelial mesenchyme transition"

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Teague, Warwick J. "Mesenchyme-to-epithelial transition in pancreatic organogenesis." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670115.

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Cheung, Pak-yan. "Esophageal carcinogenesis : immortalization, transformation and epithelial-mesenchymal transition /." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290379.

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Cheung, Pak-yan, and 張柏欣. "Esophageal carcinogenesis: immortalization, transformation and epithelial-mesenchymal transition." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290379.

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Han, ShuYi. "Histone variant H2A.Z : a master regulator of epithelial-to-mesenchymal transition." Phd thesis, Canberra, ACT : The Australian National University, 2014. http://hdl.handle.net/1885/151759.

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Robertson, Stuart. "A study of the role of splenic mesenchyme-to-epithelial transition in islet neogenesis." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/29339.

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Type 1 Diabetes Mellitus (T1DM) affects millions of children worldwide and is increasing in prevalence. Exogenous insulin therapy is currently the mainstay of treatment but is unable to prevent the chronic complications of this disease. Islet transplantation is a successful, minimally-invasive, potentially curable alternative treatment, which has restored physiological euglycaemia in up to 85% of recipients in recent clinical trials. However, worldwide human donor islet shortages limit the wider application of this treatment. Pluripotent cells may provide alternative islet sources to overcome this shortage. The human spleen may be one such source and is an excellent candidate tissue for further investigation. The main aims of this thesis were to investigate whether the developing spleen could differentiate into insulin-producing cells and to investigate the molecular mechanisms behind this. Using an avian model of pancreatic development, I characterise normal avian foregut expression of the splenic mesenchymal transcription factor Tlx-1 between E4-E11 of development and report an optimised in situ hybridisation protocol for this. I use a chick-quail chimaera model of pancreatic organogenesis to show that the developing avian spleen is able to differentiate into insulin-producing cells in vitro through islet Mesenchyme-to-Epithelial Transition (iMET). 1 show evidence that, when recombined with differentiating pancreatic epithelium, splenic mesenchyme is reprogrammed to express the pancreatic islet genes Pdx-1 and Isl-1. Tlx-1 is dramatically down-regulated during this process, indicating that this tissue is reprogrammed from a splenic to pancreatic endocrine fate. Finally, an attempt to augment splenic iMET is made through the addition of a Wnt agonist. These findings, together with the recent discovery that the mature human spleen contains Tlx-1 positive cells, may be a useful target for future bench-to-bedside translation strategies for this work. Therefore, the spleen may be an ideal future tissue source for islet transplantation to treat patients with T1DM.
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Fernández, Serra Montserrat. "Role of the MAPK signalling pathway in the epithelial mesenchyme transition in the sea urchin embryo." Thesis, Open University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441145.

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Qiao, Bin. "Epithelial-Mesenchymal Transition and Mesenchymal-Epithelial Transition in Oral Stem Cell Carcinogenesis." Thesis, Griffith University, 2011. http://hdl.handle.net/10072/367467.

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Oral squamous cell carcinoma (OSCC), derived from normal oral epithelium transformation, remains a major public health problem world-wide. The prognosis of OSCCs that occur on lips is good, while other sites of oral mucosa where OSCC appears are more progressive, invasive and metastatic. A small subset of cells within a malignant neoplasm, named cancer stem cells (CSCs) or tumour initiating cells are thought to be capable of initiating the neoplasm itself, and of driving its growth and recurrance after treatment. The precise origin of CSCs is an ambiguous issue at present. The first proposal of the origin of CSCs is that CSCs develop from tumour cells themselves via cellular dedifferentiation. The secondary hypothesis for the origin of CSCs proposes that CSCs are the product of malignant transformation of adult stem cells. In this Ph.D thesis, we tried to demonstrate that CSCs in OSCC may be produced from those pathways.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medicine
Griffith Health
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Robson, Ewan John Douglas. "Characterisation of epithelial-mesenchymal transition in murine mammary epithelial cells." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616130.

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Millanes, Romero Alba 1986. "Heterochromatin dynamics during epithelial-to-mesenchymal transition." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/129339.

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Although heterochromatin is enriched with repressive traits, it is actively transcribed, giving rise to large amounts of non-coding RNAs. These transcripts are responsible for the formation and maintenance of heterochromatin, but little is known about how their transcription is regulated. In this thesis we show that Snail1 transcription factor represses mouse pericentromeric transcription and regulates heterochromatin organization through the action of the H3K4 deaminase LOXL2. Snail1 has a key role in epithelial-to-mesenchymal transition (EMT). We show that, also during this process, Snail1 is responsible for pericentromeric transcription regulation. At the onset of EMT, one of the major structural heterochromatin proteins, HP1α, is transiently released from heterochromatin foci in a Snail1/LOXL2 dependent manner, concomitantly with a down-regulation of major satellite transcription. Moreover, prevention of major satellite transcripts down-regulation compromises the migratory and invasive behaviour of EMT resulting mesenchymal cells. We propose that Snail1 and LOXL2 regulate heterochromatin during this process, which may be crucial to allow the genome reorganization required to complete EMT.
Tot i estar enriquida en marques repressores, l’heterocromatina es transcriu activament i dóna lloc a grans quantitats d’ARNs no codificants. Aquests trànscrits són responsables de la formació i el manteniment de l’heterocromatina, però com es regula la seva transcripció segueix sent quelcom poc clarificat. En aquesta tesi demostrem que el factor de transcripció Snail1 reprimeix la transcripció pericentromèrica en cèl·lules de ratolí i regula l’organització de l’heterocromatina a través de l’acció de la LOXL2, que deamina l’H3K4. Snail1 té un paper clau en la transició epiteli-mesènquima (EMT). Aquí demostrem que, també durant aquest procés, Snail1 és responsable de la regulació de la transcripció pericentromèrica. A l’inici de l’EMT, l’HP1α, una de les principals proteïnes estructurals de l’heterocromatina, es desprèn de forma transitòria de l’heterocromatina. Aquest esdeveniment està regulat per Snail1 i LOXL2 i coincideix amb una disminució de la transcripció pericentromèrica. El bloqueig de la baixada dels trànscrits durant l’EMT compromet les capacitats migratòries i invasives de les cèl·lules mesenchimals que en resulten. Així doncs, proposem que Snail1 i LOXL2 regulen l’heterocromatina durant aquest procés, i així permeten que tingui lloc la reorganització genòmica que deu ser necessària per tal que es completi la EMT.
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Brocchieri, Cristian. "A study on the regulation of Epithelial to Mesenchymal Transition in the Ovarian Surface Epithelium." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611315.

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Books on the topic "Epithelial mesenchyme transition"

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Pierre, Savagner, ed. Rise and fall of epithelial phenotype: Concepts of epithelial-mesenchymal transition. Georgetown, Tex., U.S.A: Landes Bioscience/Eurekah.com, 2005.

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Sŏnggyun'gwan Taehakkyo (Seoul, Korea). Sanhak Hyŏmnyŏktan. TGF-beta e ŭihan oncogenic Epithelial-Mesenchymal Transition (EMT) yubal inja rosŏ hangsanhwa tanbaekchildŭl ŭi yŏkhal kyumyŏng kwa kijŏn yŏn'gu =: Molecular characterization of distinct roles of anti-oxidative proteins and their signaling mechanism in the oncogenic epithelial-mesenchymal transition by TGF-beta. [Seoul]: Pogŏn Pokchi Kajokpu, 2009.

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Muthuswamy, Senthil, John Douglas Haley, and Raghu Kalluri. Abstracts of papers presented at the 2008 meeting on epithelial-mesenchymal transition: March 17-March 20, 2008. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2008.

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Campbell, Kyra, and Eric Theveneau, eds. The Epithelial-to Mesenchymal Transition. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0779-4.

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Thompson, Erik W. Epithelial-mesenchymal transitions: new advances in development, fibrosis and cancer: 9 tables. Basel: Karger, 2011.

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Cheung, Albert. Pax3 and PAX3/FKHR induces cell aggregation and morphogenic mesenchymal-epithelial transition. Ottawa: National Library of Canada, 2002.

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Sivasubramaniyan, Kavitha. A novel antibody directed against SSEA-4 defines spontaneous epithelial-to-mesenchymal cell transition in human prostate cancer. [S.l: s.n.], 2014.

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Savagner, Pierre. Rise and Fall of Epithelial Phenotype: Concepts of Epithelial-Mesenchymal Transition (Molecular Biology Intelligence Unit). Springer, 2005.

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Savagner, Pierre. Rise and Fall of Epithelial Phenotype: Concepts of Epithelial-Mesenchymal Transition. Springer, 2010.

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Savagner, Pierre. Rise and Fall of Epithelial Phenotype: Concepts of Epithelial-Mesenchymal Transition. Springer London, Limited, 2008.

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Book chapters on the topic "Epithelial mesenchyme transition"

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Rajasekaran, Ayyappan K., and Sigrid A. Langhans. "Epithelial-to-Mesenchymal Transition." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_1962-2.

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Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "Epithelial to Mesenchymal Transition." In Encyclopedia of Signaling Molecules, 574. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100399.

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Rajasekaran, Ayyappan K., and Sigrid A. Langhans. "Epithelial-to-Mesenchymal Transition." In Encyclopedia of Cancer, 1593–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_1962.

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Rajasekaran, Ayyappan K., and Sigrid A. Rajasekaran. "Epithelial-to-Mesenchymal Transition." In Encyclopedia of Cancer, 1292–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1962.

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Choi, Yoon Jin, and Hyeon Jang. "Gastric Cancer: Epithelial Mesenchymal Transition." In Helicobacter pylori, 275–91. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-287-706-2_25.

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Van Marck, Veerle L., and Marc E. Bracke. "Epithelial-Mesenchymal Transitions in Human Cancer." In Rise and Fall of Epithelial Phenotype, 135–59. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-28671-3_9.

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Gilles, Christine, Donald F. Newgreen, Hiroshi Sato, and Erik W. Thompson. "Matrix Metalloproteases and Epithelial-to-Mesenchymal Transition." In Rise and Fall of Epithelial Phenotype, 297–315. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-28671-3_20.

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Karakas, E., J. Waldmann, G. Feldmann, K. Schlosser, A. König, A. Ramaswamy, D. K. Bartsch, and V. Fendrich. "Epithelial-mesenchymal transition in parathyroid neoplasms." In Deutsche Gesellschaft für Chirurgie, 39–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_16.

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Schmalhofer, Otto, Simone Brabletz, and Thomas Brabletz. "Epithelial-Mesenchymal Transition in Colorectal Cancer." In Metastasis of Colorectal Cancer, 147–72. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-8833-8_6.

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Davaine, Cecile, Eva Hadadi, William Taylor, Annelise Bennaceur-Griscelli, and Hervé Acloque. "Inducing Sequential Cycles of Epithelial-Mesenchymal and Mesenchymal-Epithelial Transitions in Mammary Epithelial Cells." In Methods in Molecular Biology, 341–51. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0779-4_26.

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Conference papers on the topic "Epithelial mesenchyme transition"

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Sumida, Mitsuho I., Yuichiro Tanaka, Rajvir Dahiya, and Soichiro Yamamura. "Abstract 4430: Genistein regulates non-coding RNA HOTAIR and epithelial-to-mesenchyme transition in renal cancer cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4430.

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Futterman, Matthew, and Evan A. Zamir. "A Model for Epithelial Migration and Wound Healing in the Avian Embryo." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19565.

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It is increasingly clear that (collective) migration of epithelia plays an important role in morphogenesis and wound healing [6]. One of the interesting phenomena about epithelial migration is that the leading edge of the epithelia displays characteristics of both epithelia and cells undergoing EMT (epithelial-to-mesenchymal transition), so-called “partial” EMT. Developmental models in Drosophila and zebrafish have become important for studying signaling pathways involved in epithelial migration in recent years, but it is difficult to study the biomechanics of these systems. [2] Here, we revisit a little-used developmental model originally characterized by Chernoff [3] over two decades ago, which uses the area opaca (AO) of the chick embryo, an extraembryonic epithelium in birds which normally functions to spread across and encompass the nutritive yolk in a process called epiboly. We believe this model will be useful for studying epithelial migration because it is easily accessible and can be separated from the embryo to control the biomechanical environment.
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Kroon, Jan, Onno van Hooij, Eugenio Zoni, Maaike van der Mark, Geertje van der Horst, Johan Tijhuis, Cindy van Rijt-van de Westerlo, et al. "Abstract 3768: Targeting of epithelial-to-mesenchyme transition by a novel small molecule inhibitor attenuates prostate and breast cancer invasiveness and bone metastases." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3768.

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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Brockmeyer, T., L. Pham, K. Zscheppang, S. Murray, Z. Borok, H. Nielsen, and C. Dammann. "Epithelial-Mesenchymal Transition in Fetal Type-II Epithelial Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5299.

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Wu, Tsung-Hsien, Jen-I. Liang, Yu-Wei Chiu, Ming-Long Yeh, and Chia-Hsin Chen. "Mechanical quantification of the Epithelial mesenchymal transition." In 2011 IEEE International Conference on Nano/Micro Engineered and Molecular Systems (NEMS). IEEE, 2011. http://dx.doi.org/10.1109/nems.2011.6017391.

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Yamauchi, Y., T. Kohyama, S. Kamitani, S. Kawasaki, M. Desaki, K. Takami, H. Takizawa, and T. Nagase. "Epithelial Mesenchymal Transition Modulates the Cell Proliferation of Lung Epithelial Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5306.

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Sporn, Peter H. S., Naizhen Wang, and Aisha Nair. "MicroRNA Profile Of Epithelial-Mesenchymal Transition In Normal Human Bronchial Epithelial Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2488.

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Mason, CA, and LS Brown. "Acetaldehyde Promoted Epithelial-Mesenchymal Transition through Increased TGF-β." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4971.

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Weinberg, R. "Breast Cancer Stem Cells and the Epithelial-Mesenchymal Transition." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-a1-1.

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Reports on the topic "Epithelial mesenchyme transition"

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Krause, Silva. Promotion of Epithelial to Mesenchymal Transition by Hyaluronan. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada462484.

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Krause, Silva. Promotion of Epithelial to Mesenchymal Transition by Hyaluronan. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada463843.

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Kah, Kong J. Signature and Mechanism of the Epithelial-to-Mesenchymal Transition. Fort Belvoir, VA: Defense Technical Information Center, May 2010. http://dx.doi.org/10.21236/ada541945.

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Thompson, Erik W. Functional Genomics for Epithelial-Mesenchymal Transition in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada542255.

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Kah, Kong J. Signature and Mechanism of the Epithelial-to-Mesenchymal Transition. Fort Belvoir, VA: Defense Technical Information Center, May 2009. http://dx.doi.org/10.21236/ada504655.

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Tyner, Angela L. Regulation of the Epithelial-Mesenchymal Transition in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada594294.

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Kah, Kong J. Signature and Mechanism of the Epithelial-to-Mesenchymal Transition. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada549247.

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Thompson, Erik. Functional Genomics for Epithelial-Mesenchymal Transition in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada554588.

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Peehl, Donna M. Origin of Prostate Cancer-Associated Stroma: Epithellal Mesenchymal Transition (EMT). Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada451366.

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Range, Ryan C., and Davis R. McClay. A Normal Epithelial-Mesenchymal Transition as a Model for Studying Metastatic Onset. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada416671.

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