Journal articles: '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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Vaahtokari, A., S. Vainio, and I. Thesleff. "Associations between transforming growth factor beta 1 RNA expression and epithelial-mesenchymal interactions during tooth morphogenesis." Development 113, no. 3 (November 1, 1991): 985–94. http://dx.doi.org/10.1242/dev.113.3.985.

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We have studied the expression of transforming growth factor beta-1 (TGF-beta 1) RNA during mouse tooth development, using in situ hybridization and experimental tissue recombinations. Analysis of the serial sections revealed the appearance of local expression of TGF-beta 1 RNA in the dental epithelium at bud-staged teeth (13-day embryos). Just before transition to the cap stage, TGF-beta 1 RNA expression rapidly increased in the epithelial bud, and it also extended to the condensed dental mesenchyme. At cap stage (14- and 15-day embryos), there was an intense expression of TGF-beta 1 RNA in the morphologically active cervical loops of the dental epithelium. During early bell stage (16- and 17-day embryos), TGF-beta 1 RNA expression was detected in the inner enamel epithelium where it subsequently almost disappeared (18-day embryos). After birth TGF-beta 1 transcripts transiently appeared in these cells when they were differentiating into ameloblasts (1-day mice). The transcripts were lost from the ameloblasts when they became secretory (4-day mice), but the expression continued in ameloblasts in enamel-free areas. Transient expression of TGF-beta 1 RNA was also detected in epithelial stratum intermedium cells at the time of ameloblast differentiation. In the mesenchyme, TGF-beta 1 RNA was not detected during bell stage until it appeared in differentiated odontoblasts (18-day embryos). The secretory odontoblasts continued to express TGF-beta 1 RNA at all stages studied including the odontoblasts of incisor roots. Analysis of the distribution of bromodeoxyuridine (BrdU) incorporation indicated apparent correlations between TGF-beta 1 RNA expression and cell proliferation at the bud and cap stages but not at later stages of tooth development. Tissue recombination experiments of bud-staged (13-day embryos) dental and non-dental tissues showed that tooth epithelium, when cultured together with tooth mesenchyme, expressed TGF-beta 1 RNA. When the tooth epithelium was combined with non-dental jaw mesenchyme, TGF-beta 1 transcripts were not expressed. However, TGF-beta 1 RNA expression was seen in oral epithelium cultured with dental mesenchyme, while no expression of TGF-beta 1 transcripts was seen in the oral epithelium during normal development. Thus, TGF-beta 1 RNA expression seems to be regulated by epithelial-mesenchymal interactions.

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Woolf, A. S., M. Kolatsi-Joannou, P. Hardman, E. Andermarcher, C. Moorby, L. G. Fine, P. S. Jat, M. D. Noble, and E. Gherardi. "Roles of hepatocyte growth factor/scatter factor and the met receptor in the early development of the metanephros." Journal of Cell Biology 128, no. 1 (January 1, 1995): 171–84. http://dx.doi.org/10.1083/jcb.128.1.171.

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Several lines of evidence suggest that hepatocyte growth factor/scatter factor (HGF/SF), a soluble protein secreted by embryo fibroblasts and several fibroblast lines, may elicit morphogenesis in adjacent epithelial cells. We investigated the role of HGF/SF and its membrane receptor, the product of the c-met protooncogene, in the early development of the metanephric kidney. At the inception of the mouse metanephros at embryonic day 11, HGF/SF was expressed in the mesenchyme, while met was expressed in both the ureteric bud and the mesenchyme, as assessed by reverse transcription PCR, in situ hybridization, and immunohistochemistry. To further investigate the expression of met in renal mesenchyme, we isolated 13 conditionally immortal clonal cell lines from transgenic mice expressing a temperature-sensitive mutant of the SV-40 large T antigen. Five had the HGF/SF+/met+ phenotype and eight had the HGF/SF-/met+ phenotype. None had the HGF/SF+/met- nor the HGF/SF-/met- phenotypes. Thus the renal mesenchyme contains cells that express HGF/SF and met or met alone. When metanephric rudiments were grown in serum-free organ culture, anti-HGF/SF antibodies (a) inhibited the differentiation of metanephric mesenchymal cells into the epithelial precursors of the nephron; (b) increased cell death within the renal mesenchyme; and (c) perturbed branching morphogenesis of the ureteric bud. These data provide the first demonstration for coexpression of the HGF/SF and met genes in mesenchymal cells during embryonic development and also imply an autocrine and/or paracrine role for HGF/SF and met in the survival of the renal mesenchyme and in the mesenchymal-epithelial transition that occurs during nephrogenesis. They also confirm the postulated paracrine role of HGF/SF in the branching of the ureteric bud.

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Guarino, Marcello. "Immunohistochemical Distribution of Basement Membrane Type IV Collagen and Laminin in Synovial Sarcoma." Tumori Journal 79, no. 6 (December 1993): 427–32. http://dx.doi.org/10.1177/030089169307900612.

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Aims To investigate the distribution of basement membrane components type IV collagen and laminin in synovial sarcomas. Methods Paraffin sections from four synovial sarcomas were studied by the peroxidase-antiperoxldase procedure using specific antibodies to type IV collagen and laminin. Results Type IV collagen and laminin immunoreactivity was confined around epithelial areas in biphasic tumors. Several interruptions and discontinuities of the linear basement membrane profile were seen in sites of transition between mesenchymal and epithelial tissue. Moreover, a spot-like immunoreactivity was often observed in the spindle cell component of biphasic tumors. Monophasic tumors were either negative or showed a pericellular staining for both type IV collagen and laminin. Conclusions The distribution of basement membrane components is clearly related to the formation of epithelial elements in biphasic synovial sarcoma. The spot-like immunoreactivity of the spindle cell component, and the basement membrane interruptions at the boundary between mesenchymal and epithelial tissue, are both consistent with early basement membrane formation by developing epithelium. These findings support the concept that synovial sarcomas are basically soft tissue carcinosarcomas and that the epithelial component of the tumors develops by conversion of mesenchyme to epithelium.

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Dahl, Ulf, Anders Sjödin, Lionel Larue, Glenn L. Radice, Stefan Cajander, Masatoshi Takeichi, Rolf Kemler, and Henrik Semb. "Genetic Dissection of Cadherin Function during Nephrogenesis." Molecular and Cellular Biology 22, no. 5 (March 1, 2002): 1474–87. http://dx.doi.org/10.1128/mcb.22.5.1474-1487.2002.

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ABSTRACT The distinct expression of R-cadherin in the induced aggregating metanephric mesenchyme suggests that it may regulate the mesenchymal-epithelial transition during kidney development. To address whether R-cadherin is required for kidney ontogeny, R-cadherin-deficient mice were generated. These mice appeared to be healthy and were fertile, demonstrating that R-cadherin is not essential for embryogenesis. The only kidney phenotype of adult mutant animals was the appearance of dilated proximal tubules, which was associated with an accumulation of large intracellular vacuoles. Morphological analysis of nephrogenesis in R-cadherin −/− mice in vivo and in vitro revealed defects in the development of both ureteric bud-derived cells and metanephric mesenchyme-derived cells. First, the morphology and organization of the proximal parts of the ureteric bud epithelium were altered. Interestingly, these morphological changes correlated with an increased rate of apoptosis and were further supported by perturbed branching and patterning of the ureteric bud epithelium during in vitro differentiation. Second, during in vitro studies of mesenchymal-epithelial conversion, significantly fewer epithelial structures developed from R-cadherin −/− kidneys than from wild-type kidneys. These data suggest that R-cadherin is functionally involved in the differentiation of both mesenchymal and epithelial components during metanephric kidney development. Finally, to investigate whether the redundant expression of other classic cadherins expressed in the kidney could explain the rather mild kidney defects in R-cadherin-deficient mice, we intercrossed R-cadherin −/− mice with cadherin-6−/− , P-cadherin −/−, and N-cadherin +/− mice. Surprisingly, however, in none of the compound knockout strains was kidney development affected to a greater extent than within the individual cadherin knockout strains.

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Choi, Steve S., Alessia Omenetti, Rafal P. Witek, Cynthia A. Moylan, Wing-Kin Syn, Youngmi Jung, Liu Yang, et al. "Hedgehog pathway activation and epithelial-to-mesenchymal transitions during myofibroblastic transformation of rat hepatic cells in culture and cirrhosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 6 (December 2009): G1093—G1106. http://dx.doi.org/10.1152/ajpgi.00292.2009.

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Myofibroblastic hepatic stellate cells (MF-HSC) are derived from quiescent hepatic stellate cells (Q-HSC). Q-HSC express certain epithelial cell markers and have been reported to form junctional complexes similar to epithelial cells. We have shown that Hedgehog (Hh) signaling plays a key role in HSC growth. Because Hh ligands regulate epithelial-to-mesenchymal transition (EMT), we determined whether Q-HSC express EMT markers and then assessed whether these markers change as Q-HSC transition into MF-HSC and whether the process is modulated by Hh signaling. Q-HSC were isolated from healthy livers and cultured to promote myofibroblastic transition. Changes in mRNA and protein expression of epithelial and mesenchymal markers, Hh ligands, and target genes were monitored in HSC treated with and without cyclopamine (an Hh inhibitor). Studies were repeated in primary human HSC and clonally derived HSC from a cirrhotic rat. Q-HSC activation in vitro (culture) and in vivo (CCl4-induced cirrhosis) resulted in decreased expression of Hh-interacting protein (Hhip, an Hh antagonist), the EMT inhibitors bone morphogenic protein (BMP-7) and inhibitor of differentiation (Id2), the adherens junction component E-cadherin, and epithelial keratins 7 and 19 and increased expression of Gli2 (an Hh target gene) and mesenchymal markers, including the mesenchyme-associated transcription factors Lhx2 and Msx2, the myofibroblast marker α-smooth muscle actin, and matrix molecules such as collagen. Cyclopamine reverted myofibroblastic transition, reducing mesenchymal gene expression while increasing epithelial markers in rodent and human HSC. We conclude that Hh signaling plays a key role in transition of Q-HSC into MF-HSC. Our findings suggest that Q-HSC are capable of transitioning between epithelial and mesenchymal fates.

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Teague, Warwick J., Autumn M. Rowan-Hull, Naga V. G. Jayanthi, and Paul R. V. Johnson. "The competency of foregut mesenchyme in islet mesenchyme-to-epithelial transition during embryonic development." Journal of Pediatric Surgery 41, no. 2 (February 2006): 347–51. http://dx.doi.org/10.1016/j.jpedsurg.2005.11.011.

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Yeh, Yi-Chun, Hsi-Hui Lin, and Ming-Jer Tang. "A tale of two collagen receptors, integrin β1 and discoidin domain receptor 1, in epithelial cell differentiation." American Journal of Physiology-Cell Physiology 303, no. 12 (December 15, 2012): C1207—C1217. http://dx.doi.org/10.1152/ajpcell.00253.2012.

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As increase in collagen deposition is no longer taken as simply a consequence but, rather, an inducer of disease progression; therefore, the understanding of collagen signal transduction is fundamentally important. Cells contain at least two types of collagen receptors: integrins and discoidin domain receptors (DDRs). The integrin heterodimers α1β1, α2β1, α10β1, and α11β1 are recognized as the non-tyrosine kinase collagen receptors. DDR1 and 2, the tyrosine kinase receptors of collagen, are specifically expressed in epithelium and mesenchyme, respectively. While integrin β1 and DDR1 are both required for cell adhesion on collagen, their roles in epithelial cell differentiation during development and disease progression seem to counteract each other, with integrin β1 favoring epithelium mesenchyme transition (EMT) and DDR1 inducing epithelial cell differentiation. The in vitro evidence shows that the integrin β1 and DDR1 exert opposing actions in regulation of membrane stability of E-cadherin, which itself is a critical regulator of epithelial cell differentiation. Here, we review the functional roles of integrin β1 and DDR1 in regulation of epithelial cell differentiation during development and disease progression, and explore the underlining mechanisms regarding to the regulation of membrane stability of E-cadherin.

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Horster, Michael F., Gerald S. Braun, and Stephan M. Huber. "Embryonic Renal Epithelia: Induction, Nephrogenesis, and Cell Differentiation." Physiological Reviews 79, no. 4 (January 10, 1999): 1157–91. http://dx.doi.org/10.1152/physrev.1999.79.4.1157.

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Embryonic metanephroi, differentiating into the adult kidney, have come to be a generally accepted model system for organogenesis. Nephrogenesis implies a highly controlled series of morphogenetic and differentiation events that starts with reciprocal inductive interactions between two different primordial tissues and leads, in one of two mainstream processes, to the formation of mesenchymal condensations and aggregates. These go through the intricate process of mesenchyme-to-epithelium transition by which epithelial cell polarization is initiated, and they continue to differentiate into the highly specialized epithelial cell populations of the nephron. Each step along the developmental metanephrogenic pathway is initiated and organized by signaling molecules that are locally secreted polypeptides encoded by different gene families and regulated by transcription factors. Nephrogenesis proceeds from the deep to the outer cortex, and it is directed by a second, entirely different developmental process, the ductal branching of the ureteric bud-derived collecting tubule. Both systems, the nephrogenic (mesenchymal) and the ductogenic (ureteric), undergo a repeat series of inductive signaling that serves to organize the architecture and differentiated cell functions in a cascade of developmental gene programs. The aim of this review is to present a coherent picture of principles and mechanisms in embryonic renal epithelia.

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Brakeman, Paul R., Kathleen D. Liu, Kazuya Shimizu, Yoshimi Takai, and Keith E. Mostov. "Nectin proteins are expressed at early stages of nephrogenesis and play a role in renal epithelial cell morphogenesis." American Journal of Physiology-Renal Physiology 296, no. 3 (March 2009): F564—F574. http://dx.doi.org/10.1152/ajprenal.90328.2008.

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Development of the nephron requires conversion of the metanephric mesenchyme into tubular epithelial structures with specifically organized intercellular junctions. The nectin proteins are a family of transmembrane proteins that dimerize to form intercellular junctional complexes between epithelial cells. In this study, we demonstrate that nectin junctions appear during the earliest stages of epithelial cell morphogenesis in the murine nephron concurrently with the transition of mesenchymal cells into epithelial cells. We have defined the role of nectin during epithelial cell morphogenesis by studying nectin in a three-dimensional culture of Madin-Darby canine kidney (MDCK) cells. In a three-dimensional culture of MDCK cells grown in purified type 1 collagen, expression of a dominant negative form of nectin causes disruption of the formation of cell polarity and disruption of tight junction (TJ) formation, as measured by zonula occludens-1 (ZO-1) localization. In MDCK cells cultured in Matrigel, exogenous expression of nectin-1 causes disruption of normal epithelial cell cyst formation and decreased apoptosis. These data demonstrate that nectins play an important role in normal epithelial cell morphogenesis and may play a role in mesenchymal-to-epithelial transition during nephrogenesis by providing an antiapoptotic signal and promoting the formation of TJs and cell polarity.

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Nagaoka, K., K. Fujii, H. Zhang, K. Usuda, G. Watanabe, M. Ivshina, and J. D. Richter. "CPEB1 mediates epithelial-to-mesenchyme transition and breast cancer metastasis." Oncogene 35, no. 22 (September 28, 2015): 2893–901. http://dx.doi.org/10.1038/onc.2015.350.

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Robertson, Stuart, Paul D’Alessandro, Autumn Rowan-Hull, Raina Ramnath, and Paul Johnson. "14-P006 Splenic mesenchyme-to-epithelial transition in islet neogenesis." Mechanisms of Development 126 (August 2009): S240—S241. http://dx.doi.org/10.1016/j.mod.2009.06.625.

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Pungchanchaikul, P., M. Gelbier, P. Ferretti, and A. Bloch-Zupan. "Gene Expression during Palate Fusion in vivo and in vitro." Journal of Dental Research 84, no. 6 (June 2005): 526–31. http://dx.doi.org/10.1177/154405910508400608.

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Failure of secondary palate fusion during embryogenesis is a cause of cleft palate. Disappearance of the medial epithelial seam (MES) is required to allow merging of the mesenchyme from both palatal shelves. This involves complex changes of the medial edge epithelial (MEE) cells and surrounding structures that are controlled by several genes whose spatio-temporal expression is tightly regulated. We have carried out morphological analyses and used a semi-quantitative RT-PCR technique to evaluate whether morphological changes and modulation in the expression of putative key genes, such as twist, snail, and E-cadherin, during the fusion process in palate organ culture parallel those observed in vivo, and show that this is indeed the case. We also show, using the organotypic model of palate fusion, that the down-regulation of the transcription factor snail that occurs with the progression of palate development is not dependent on fusion of the palatal shelves. Abbreviations: dsg1, desmoglein1; EMT, epithelial-mesenchymal transition; MEE, medial edge epithelium; MES, medial epithelial seam; RT-PCR, reverse-transcriptase polymerase chain-reaction.

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Jayanthi, N. V. G., A. M. Rowan-Hull, W. J. Teague, and P. R. V. Johnson. "The Importance of Pancreatic Embryonic Epithelium for Mesenchyme-to-Epithelial Transition During Islet Development." Transplantation Proceedings 37, no. 8 (October 2005): 3485–86. http://dx.doi.org/10.1016/j.transproceed.2005.09.026.

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Frumkin, A., G. Pillemer, R. Haffner, N. Tarcic, Y. Gruenbaum, and A. Fainsod. "A role for CdxA in gut closure and intestinal epithelia differentiation." Development 120, no. 2 (February 1, 1994): 253–63. http://dx.doi.org/10.1242/dev.120.2.253.

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CdxA is a homeobox gene of the caudal type that was previously shown to be expressed in the endoderm-derived gut epithelium during early embryogenesis. Expression of the CDXA protein was studied during intestine morphogenesis from stage 11 (13 somites) to adulthood in the chicken. The CDXA protein can be detected during all stages of gut closure, from stage 11 to 5 days of incubation, and is mainly localized to the intestinal portals, the region where the splanchnopleure is undergoing closure. In this region, which represents the transition between the open and closed gut, the CDXA protein is restricted to the endoderm-derived epithelium. At about day 5 of incubation, the process of formation of the previllous ridges begins, which marks the beginning of the morphogenesis of the villi. From this stage to day 11 expression of CDXA is localized to the epithelial lining of the intestine. In parallel, a gradual increase in CDXA protein expression begins in the mesenchyme that is close in proximity to the CDXA-positive endoderm. Maximal CDXA levels in the mesenchyme are observed at day 9 of incubation. During days 10 and 11 CDXA levels in the mesenchyme remain constant, and by day 12 CDXA becomes undetectable in these cells and the epithelium again becomes the main site of expression. From day 12 of incubation until adulthood the CDXA protein is present in the intestinal epithelium. Until day 18 of incubation expression can be detected along the whole length of the villus with a stronger signal at the tip. With hatching the distribution along the villi changes so that the main site of CDXA protein expression is at the base of the villi and in the crypts. The transient expression of CDXA in the mesenchyme between days 5 and 11 may be related to the interactions taking place between the mesenchyme and the epithelium that ultimately result in the axial specification of the alimentary canal and the differentiation of its various epithelia. The main CDXA spatial distribution during morphogenesis suggests a tight linkage to the formation and differentiation of the intestinal epithelium itself. CDXA appears to play a role in the morphogenetic events leading to closure of the alimentary canal. During previllous ridge formation the CDXA protein is transiently expressed in the mesenchymal cells thought to provide instructive interactions for the regionalization and differentiation of the gut epithelium.(ABSTRACT TRUNCATED AT 400 WORDS)

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Hirano, Mariko, and Shinichi Aizawa. "Arf6 recruits EPB41L5 for E-cadherin endocytosis during epithelial–mesenchyme transition." Developmental Biology 344, no. 1 (August 2010): 509. http://dx.doi.org/10.1016/j.ydbio.2010.05.346.

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Bloch, Julie, Marc Hazzan, Cynthia Van der Hauwaert, David Buob, Grégoire Savary, Alexandre Hertig, Viviane Gnemmi, et al. "DonorABCB1genetic polymorphisms influence epithelial-to-mesenchyme transition in tacrolimus-treated kidney recipients." Pharmacogenomics 15, no. 16 (December 2014): 2011–24. http://dx.doi.org/10.2217/pgs.14.146.

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Zhu, Liang, and Ying Ding. "RGC-32 induces transition of pancreatic cancer to epithelial mesenchyme in vivo." Pancreatology 18, no. 5 (July 2018): 572–76. http://dx.doi.org/10.1016/j.pan.2018.05.480.

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Hirano, M., and S. Aizawa. "P12. Arf6 recruits EPB41L5 for E-cadherin endocytosis during epithelial–mesenchyme transition." Differentiation 80 (November 2010): S21. http://dx.doi.org/10.1016/j.diff.2010.09.018.

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Wu, Shu-Yu, Michael Ferkowicz, and David R. McClay. "Ingression of primary mesenchyme cells of the sea urchin embryo: A precisely timed epithelial mesenchymal transition." Birth Defects Research Part C: Embryo Today: Reviews 81, no. 4 (December 2007): 241–52. http://dx.doi.org/10.1002/bdrc.20113.

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Baraniak, Andrew P., Jing R. Chen, and Mariano A. Garcia-Blanco. "Fox-2 Mediates Epithelial Cell-Specific Fibroblast Growth Factor Receptor 2 Exon Choice." Molecular and Cellular Biology 26, no. 4 (February 15, 2006): 1209–22. http://dx.doi.org/10.1128/mcb.26.4.1209-1222.2006.

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ABSTRACT Alternative splicing of fibroblast growth factor receptor 2 (FGFR2) transcripts occurs in a cell-type-specific manner leading to the mutually exclusive use of exon IIIb in epithelia or exon IIIc in mesenchyme. Epithelial cell-specific exon choice is dependent on (U)GCAUG elements, which have been shown to bind Fox protein family members. In this paper we show that FGFR2 exon choice is regulated by (U)GCAUG elements and Fox protein family members. Fox-2 isoforms are differentially expressed in IIIb+ cells in comparison to IIIc+ cells, and expression of Fox-1 or Fox-2 in the latter led to a striking alteration in FGFR2 splice choice from IIIc to IIIb. This switch was absolutely dependent on the (U)GCAUG elements present in the FGFR2 pre-mRNA and required critical residues in the C-terminal region of Fox-2. Interestingly, Fox-2 expression led to skipping of exon 6 among endogenous Fox-2 transcripts and formation of an inactive Fox-2 isoform, which suggests that Fox-2 can regulate its own activity. Moreover, the repression of exon IIIc in IIIb+ cells was abrogated by interfering RNA-mediated knockdown of Fox-2. We also show that Fox-2 is critical for the FGFR2(IIIb)-to-FGFR2(IIIc) switch observed in T Rex-293 cells grown to overconfluency. Overconfluent T Rex-293 cells show molecular and morphological changes consistent with a mesenchymal-to-epithelial transition. If overconfluent cells are depleted of Fox-2, the switch from IIIc to IIIb is abrogated. The data in this paper place Fox-2 among critical regulators of gene expression during mesenchymal-epithelial transitions and demonstrate that this action of Fox-2 is mediated by mechanisms distinct from those described for other cases of Fox activity.

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Buckley, Stephen T., Carlos Medina, Michael Kasper, and Carsten Ehrhardt. "Interplay between RAGE, CD44, and focal adhesion molecules in epithelial-mesenchymal transition of alveolar epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 300, no. 4 (April 2011): L548—L559. http://dx.doi.org/10.1152/ajplung.00230.2010.

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Fibrosis of the lung is characterized by the accumulation of myofibroblasts, a key mediator in the fibrogenic reaction. Cumulative evidence indicates that epithelial-mesenchymal transition (EMT), a process whereby epithelial cells become mesenchyme-like, is an important contributing source for the myofibroblast population. Underlying this phenotypical change is a dramatic alteration in cellular structure. The receptor for advanced glycation end-products (RAGE) has been suggested to maintain lung homeostasis by mediating cell adhesion, while the family of ezrin/radixin/moesin (ERM) proteins, on the other hand, serve as an important cross-linker between the plasma membrane and cytoskeleton. In the present investigation, we tested the hypothesis that RAGE and ERM interact and play a key role in regulating EMT-associated structural changes in alveolar epithelial cells. Exposure of A549 cells to inflammatory cytokines resulted in phosphorylation and redistribution of ERM to the cell periphery and localization with EMT-related actin stress fibers. Simultaneously, blockade of Rho kinase (ROCK) signaling attenuated these cytokine-induced structural changes. Additionally, RAGE expression was diminished after cytokine stimulation, with release of its soluble isoform via a matrix metalloproteinase (MMP)-9-dependent mechanism. Immunofluorescence microscopy and coimmunoprecipitation revealed association between ERM and RAGE under basal conditions, which was disrupted when challenged with inflammatory cytokines, as ERM in its activated state complexed with membrane-linked CD44. Dual-fluorescence immunohistochemistry of patient idiopathic pulmonary fibrosis (IPF) tissues highlighted marked diminution of RAGE in fibrotic samples, together with enhanced levels of CD44 and double-positive cells for CD44 and phospho (p)ERM. These data suggest that dysregulation of the ERM-RAGE complex might be an important step in rearrangement of the actin cytoskeleton during proinflammatory cytokine-induced EMT of human alveolar epithelial cells.

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Cano, Elena, Rita Carmona, and Ramón Muñoz-Chápuli. "Wt1-expressing progenitors contribute to multiple tissues in the developing lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 4 (August 15, 2013): L322—L332. http://dx.doi.org/10.1152/ajplung.00424.2012.

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Lungs develop from paired endodermal outgrowths surrounded by a mesodermal mesenchyme. Part of this mesenchyme arises from epithelial-mesenchymal transition of the mesothelium that lines the pulmonary buds. Previous studies have shown that this mesothelium-derived mesenchyme contributes to the smooth muscle of the pulmonary vessels, but its significance for lung morphogenesis and its developmental fate are still little known. We have studied this issue using the transgenic mouse model mWt1/IRES/GFP-Cre (Wt1cre) crossed with the Rosa26R-EYFP reporter mouse. In the developing lungs, Wt1, the Wilms' tumor suppressor gene, is specifically expressed in the embryonic mesothelium. In the embryos obtained from the crossbreeding, the Wt1-expressing cell lineage produces the yellow fluorescent protein (YFP), allowing for colocalization with differentiation markers. Wt1cre-YFP cells were very abundant from the origin of the lung buds to postnatal stages, contributing significantly to pulmonary endothelial and smooth muscle cells, bronchial musculature, tracheal and bronchial cartilage, as well as CD34+ fibroblast-like interstitial cells. Thus Wt1cre-YFP mesenchymal cells show the very same differentiation potential as the splanchnopleural mesenchyme surrounding the lung buds. FSP1+ fibroblast-like cells were always YFP−; they expressed the common leukocyte antigen CD45 and were apparently recruited from circulating progenitors. We have also found defects in pulmonary development in Wt1−/− embryos, which showed abnormally fused lung lobes, round-shaped and reduced pleural cavities, and diaphragmatic hernia. Our results suggest a novel role for the embryonic mesothelium-derived cells in lung morphogenesis and involve the Wilms' tumor suppressor gene in the development of this organ.

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Yi, Jin-Kyu, Shebli Mehrazarin, Ju-Eun Oh, Anu Bhalla, Jenessa Oo, Wei Chen, Min Lee, et al. "Osteo-/Odontogenic Differentiation of Induced Mesenchymal Stem Cells Generated through Epithelial–Mesenchyme Transition of Cultured Human Keratinocytes." Journal of Endodontics 40, no. 11 (November 2014): 1796–801. http://dx.doi.org/10.1016/j.joen.2014.07.014.

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34

Krubasik, D., N. G. Iyer, W. R. English, A. A. Ahmed, M. Vias, C. Roskelley, J. D. Brenton, C. Caldas, and G. Murphy. "Absence of p300 induces cellular phenotypic changes characteristic of epithelial to mesenchyme transition." British Journal of Cancer 94, no. 9 (April 18, 2006): 1326–32. http://dx.doi.org/10.1038/sj.bjc.6603101.

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35

Thesleff, Irma, Soile Keranen, and Jukka Jernvall. "Enamel Knots as Signaling Centers Linking Tooth Morphogenesis and Odontoblast Differentiation." Advances in Dental Research 15, no. 1 (August 2001): 14–18. http://dx.doi.org/10.1177/08959374010150010401.

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Odontoblasts differentiate from the cells of the dental papilla, and it has been well-established that their differentiation in developing teeth is induced by the dental epithelium. In experimental studies, no other mesenchymal cells have been shown to have the capacity to differentiate into odontoblasts, indicating that the dental papilla cells have been committed to odontoblast cell lineage during earlier developmental stages. We propose that the advancing differentiation within the odontoblast cell lineage is regulated by sequential epithelial signals. The first epithelial signals from the early oral ectoderm induce the odontogenic potential in the cranial neural crest cells. The next step in the determination of the odontogenic cell lineage is the development of the dental papilla from odontogenic mesenchyme. The formation of the dental papilla starts at the onset of the transition from the bud to the cap stage of tooth morphogenesis, and this is regulated by epithelial signals from the primary enamel knot. The primary enamel knot is a signaling center which forms at the tip of the epithelial tooth bud. It becomes fully developed and morphologically discernible in the cap-stage dental epithelium and expresses at least ten different signaling molecules belonging to the BMP, FGF, Hh, and Wnt families. In molar teeth, secondary enamel knots appear in the enamel epithelium at the sites of the future cusps. They also express several signaling molecules, and their formation precedes the folding and growth of the epithelium. The differentiation of odontoblasts always starts from the tips of the cusps, and therefore, it is conceivable that some of the signals expressed in the enamel knots may act as inducers of odontoblast differentiation. The functions of the different signals in enamel knots are not precisely known. We have shown that FGFs stimulate the proliferation of mesenchymal as well as epithelial cells, and they may also regulate the growth of the cusps. We have proposed that the enamel knot signals also have important roles, together with mesenchymal signals, in regulating the patterning of the cusps and hence the shape of the tooth crown. We suggest that the enamel knots are central regulators of tooth development, since they link cell differentiation to morphogenesis.

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Krubasik, D., N. G. Iyer, W. R. English, A. A. Ahmed, M. Vias, C. Roskelley, J. D. Brenton, C. Caldas, and G. Murphy. "Erratum: Absence of p300 induces cellular phenotypic changes characteristic of epithelial to mesenchyme transition." British Journal of Cancer 95, no. 2 (July 2006): 245. http://dx.doi.org/10.1038/sj.bjc.6603202.

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Duband, Jean-Loup, Cédrine Blavet, Artem Jarov, and Claire Fournier-Thibault. "Spatio-temporal control of neural epithelial cell migration and epithelium-to-mesenchyme transition during avian neural tube development." Development, Growth & Differentiation 51, no. 1 (December 26, 2008): 25–44. http://dx.doi.org/10.1111/j.1440-169x.2009.01076.x.

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Yamada, S., R. Lav, J. Li, A. S. Tucker, and J. B. A. Green. "Molar Bud-to-Cap Transition Is Proliferation Independent." Journal of Dental Research 98, no. 11 (August 8, 2019): 1253–61. http://dx.doi.org/10.1177/0022034519869307.

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Tooth germs undergo a series of dynamic morphologic changes through bud, cap, and bell stages, in which odontogenic epithelium continuously extends into the underlying mesenchyme. During the transition from the bud stage to the cap stage, the base of the bud flattens and then bends into a cap shape whose edges are referred to as “cervical loops.” Although genetic mechanisms for cap formation have been well described, little is understood about the morphogenetic mechanisms. Computer modeling and cell trajectory tracking have suggested that the epithelial bending is driven purely by differential cell proliferation and adhesion in different parts of the tooth germ. Here, we show that, unexpectedly, inhibition of cell proliferation did not prevent bud-to-cap morphogenesis. We quantified cell shapes and actin and myosin distributions in different parts of the tooth epithelium at the critical stages and found that these are consistent with basal relaxation in the forming cervical loops and basal constriction around enamel knot at the center of the cap. Inhibition of focal adhesion kinase, which is required for basal constriction in other systems, arrested the molar explant morphogenesis at the bud stage. Together, these results show that the bud-to-cap transition is largely proliferation independent, and we propose that it is driven by classic actomyosin-driven cell shape–dependent mechanisms. We discuss how these results can be reconciled with the previous models and data.

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Grego-Bessa, Joaquín, Juan Díez, and José Luis de la Pompa. "Notch and Epithelial-Mesenchyme Transition in Development and Tumor Progression: Another Turn of the Screw." Cell Cycle 3, no. 6 (June 2004): 716–19. http://dx.doi.org/10.4161/cc.3.6.949.

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Xu, Ying, and Qing Zhu. "Histone Modifications Represent a Key Epigenetic Feature of Epithelial-to-Mesenchyme Transition in Pancreatic Cancer." International Journal of Molecular Sciences 24, no. 5 (March 2, 2023): 4820. http://dx.doi.org/10.3390/ijms24054820.

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Pancreatic cancer is one of the most lethal malignant diseases due to its high invasiveness, early metastatic properties, rapid disease progression, and typically late diagnosis. Notably, the capacity for pancreatic cancer cells to undergo epithelial–mesenchymal transition (EMT) is key to their tumorigenic and metastatic potential, and is a feature that can explain the therapeutic resistance of such cancers to treatment. Epigenetic modifications are a central molecular feature of EMT, for which histone modifications are most prevalent. The modification of histones is a dynamic process typically carried out by pairs of reverse catalytic enzymes, and the functions of these enzymes are increasingly relevant to our improved understanding of cancer. In this review, we discuss the mechanisms through which histone-modifying enzymes regulate EMT in pancreatic cancer.

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Higgins, S., S. H. X. Wong, M. Richner, C. L. Rowe, D. F. Newgreen, G. A. Werther, and V. C. Russo. "Fibroblast Growth Factor 2 Reactivates G1 Checkpoint in SK-N-MC Cells via Regulation of p21, Inhibitor of Differentiation Genes (Id1-3), and Epithelium-Mesenchyme Transition-Like Events." Endocrinology 150, no. 9 (May 28, 2009): 4044–55. http://dx.doi.org/10.1210/en.2008-1797.

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Abstract We have recently demonstrated that fibroblast growth factor (FGF)-2 promotes neuroblastoma cell differentiation and overrides their mitogenic response to IGF-I. However, the mechanisms involved are unknown. SK-N-MC cells were cultured with FGF-2 (50 ng/ml) and/or IGF-I (100 ng/ml) up to 48 h. Fluorescence-activated cell sorting analysis indicated that FGF-2 promotes G1/G0 cell cycle phase arrest. Gene expression by RT2-PCR and cellular localization showed up-regulation of p21. We then investigated whether FGF-2-induced differentiation of SK-N-MC cells (by GAP43 and NeuroD-6 expression) involves epithelium-mesenchyme transition interconversion. Real-time PCR (RT2-PCR) showed modulation of genes involved in maintenance of the epithelial phenotype and cell-matrix interactions (E-cadherin, Snail-1, MMPs). Zymography confirmed FGF-2 up-regulated MMP2 and induced MMP9, known to contribute to neuronal differentiation and neurite extension. Id1-3 expression was determined by RT2-PCR. FGF-2 induced Id2, while down-regulating Id1 and Id3. FGF-2 induced nuclear accumulation of ID2 protein, while ID1 and ID3 remained cytoplasmic. RNA interference demonstrated that Id3 regulates differentiation and cell cycle (increased Neuro-D6 and p21 mRNA), while d Id2 modulates epithelium-mesenchyme transition-like events (increased E-cadherin mRNA). In conclusion, we have shown for the first time that FGF-2 induces differentiation of neuroblastoma cells via activation of a complex gene expression program enabling modulation of cell cycle, transcription factors, and suppression of the cancer phenotype. The use of RNA interference indicated that Id-3 is a key regulator of these events, thus pointing to a novel therapeutic target for this devastating childhood cancer.

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Teague, Warwick J., Aatumn M. Rowan-Hull, and Paul R. V. Johnson. "Pancreatic α-cell differentiation by mesenchyme-to-epithelial transition: implications for cell-based therapies in children." Journal of Pediatric Surgery 42, no. 1 (January 2007): 153–59. http://dx.doi.org/10.1016/j.jpedsurg.2006.09.045.

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Liu, Zhizhong, Bairong Fang, Jian Cao, Qianyin Zhou, Fang Zhu, Liqing Fan, Lei Xue, Chuan Huang, and Hao Bo. "LINC00313 regulates the metastasis of testicular germ cell tumors through epithelial-mesenchyme transition and immune pathways." Bioengineered 13, no. 5 (May 2, 2022): 12141–55. http://dx.doi.org/10.1080/21655979.2022.2073128.

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Giudice, Fernanda S., Decio S. Pinto, Jacques E. Nör, Cristiane H. Squarize, and Rogerio M. Castilho. "Inhibition of Histone Deacetylase Impacts Cancer Stem Cells and Induces Epithelial-Mesenchyme Transition of Head and Neck Cancer." PLoS ONE 8, no. 3 (March 20, 2013): e58672. http://dx.doi.org/10.1371/journal.pone.0058672.

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Yang, Zhibo, Suresh Rayala, Diep Nguyen, Ratna K. Vadlamudi, Shiuan Chen, and Rakesh Kumar. "Pak1 Phosphorylation of Snail, a Master Regulator of Epithelial-to-Mesenchyme Transition, Modulates Snail's Subcellular Localization and Functions." Cancer Research 65, no. 8 (April 15, 2005): 3179–84. http://dx.doi.org/10.1158/0008-5472.can-04-3480.

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Liu, Z., T. Chen, D. Bai, W. Tian, and Y. Chen. "Smad7 Regulates Dental Epithelial Proliferation during Tooth Development." Journal of Dental Research 98, no. 12 (September 9, 2019): 1376–85. http://dx.doi.org/10.1177/0022034519872487.

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Tooth morphogenesis involves dynamic changes in shape and size as it proceeds through the bud, cap, and bell stages. This process requires exact regulation of cell proliferation and differentiation. Smad7, a general antagonist against transforming growth factor–β (TGF-β) signaling, is necessary for maintaining homeostasis and proper functionality in many organs. While TGF-β signaling is widely involved in tooth morphogenesis, the precise role of Smad7 in tooth development remains unknown. In this study, we showed that Smad7 is expressed in the developing mouse molars with a high level in the dental epithelium but a moderate to weak level in the dental mesenchyme. Smad7 deficiency led to a profound decrease in tooth size primarily due to a severely compromised cell proliferation capability in the dental epithelium. Consistent with the tooth shrinkage phenotype, RNA sequencing (RNA-seq) analysis revealed that Smad7 ablation downregulated genes referred to epithelial cell proliferation and cell cycle G1/S phase transition, whereas the upregulated genes were involved in responding to TGF-β signaling and cell cycle arrest. Among these genes, the expression of Cdkn1a (encoding p21), a negative cell proliferation regulator, was remarkably elevated in parallel with the diminution of Ccnd1 encoding the crucial cell cycle regulator cyclin D1 in the dental epithelium. Meanwhile, the expression level of p-Smad2/3 was ectopically elevated in the developing tooth germ of Smad7 null mice, indicating the hyperactivation of the canonical TGF-β signaling. These effects were reversed by addition of TGF-β signaling inhibitor in cell cultures of Smad7−/− molar tooth germs, with rescued expression of cyclin D1 and cell proliferation rate. In sum, our studies demonstrate that Smad7 functions primarily as a positive regulator of cell proliferation via inhibition of the canonical TGF-β signaling during dental epithelium development and highlight a crucial role for Smad7 in regulating tooth size.

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Trirahmanto, Addin, Hariyono Winarto, Aria Kekalih, and Ferry Sandra. "Plasma MicroRNA-200c as A Prognostic Biomarker for Epithelial Ovarian Cancer." Indonesian Biomedical Journal 11, no. 3 (December 3, 2019): 267–72. http://dx.doi.org/10.18585/inabj.v11i3.761.

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BACKGROUND: Ovarian cancer is the 8th most prevalent cancer in women in the world. Current biomarker prognosis for ovarian cancer has numerous limitations, thus new biomarkers are needed. MicroRNAs (miRs) are considered as potential biomarkers in ovarian cancer as they are stable in blood. One candidate is miR-200c, the main regulator in epithelial transition to the mesenchyme. The aim of this study is to determine the role of miR-200c as prognostic biomarker for epithelial ovarian cancer (EOC).METHODS: This is a prospective cohort study conducted at Dr. Sardjito Central General Hospital in Yogyakarta from September 2015 to July 2018. Sampling was done using consecutive sampling method. Forty plasma samples of EOC subjects were included in this study. miR-200c expression was quantified using Reverse Transcriptase Quantitative Quantitative Polymerase Chain Reaction (RTqPCR) with miR-16 as the reference gene.RESULTS: The expression of miR-200c was significantly higher in the group of subjects with preoperative CA-125 levels >500 U/mL (p=0.009) than the group of subjects with preoperative CA-125 levels <500 U/mL. Subjects with higher miR-200c expression had lower survival rate than subjects with lower miR-200c expression, although not statistically significant.CONCLUSION: The miR-200c could be a promising biomarker for EOC. Further studies with larger sample sizes are needed to clarify the prognostic value of miR200c.KEYWORDS: miR-200c, epithelial ovarian cancer, prognosis, overall survival

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Xue, C., P. R. Reynolds, and R. A. Johns. "Developmental expression of NOS isoforms in fetal rat lung: implications for transitional circulation and pulmonary angiogenesis." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 1 (January 1, 1996): L88—L100. http://dx.doi.org/10.1152/ajplung.1996.270.1.l88.

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To better understand the role of nitric oxide (NO) in fetal lung development, specifically in the transition of the fetal circulation at birth, we studied the timing of cell-specific expression of NO synthase (NOS) isoforms from formation of lung buds (13th day of gestation) to 7 days postnatal. Expression of NOS was studied using immunohistochemical labeling with antibodies against the three known NOS isoforms and the NADPH diaphorase technique (NADPH-d). Endothelial NOS (eNOS) immunoreactivity was found in the cells of the 14-day fetal lung. As gestation proceeded, the quantity of these immunopositive cells increased, and they coalesced to form an inner (endothelial) layer of pulmonary vessels. This process of angiogenesis marked by eNOS-positive cells was seen from 15 days of gestation to at least 7 days postnatal. A majority of the eNOS immunoreactivity appeared densely in one focal spot in the cytoplasm, indicating that during development the eNOS may be primarily located in a cytoplasmic organelle. Epithelial cells of the rat airway from the same developmental period were positively stained with both brain NOS antibody (bNOS) and NADPH-d at the beginning of 13 days of gestation. Then the intensity of stainings began to decrease and reached the lowest level in the 16-day fetal lung. However, the NOS stainings of the epithelium, especially in small canalicular structures of the airways, began to increase at 18 days of gestation and was dramatically elevated at 20 days of gestation (term is 22 days). Postnatally, NOS in epithelium was decreased in distal airways in conjunction with the formation of alveolar structure. Inducible NOS (iNOS) immunoreactivity was also found in the epithelium of rat lung airways after 16 days of gestation. Unlike the bNOS staining, iNOS immunoreactivity exhibited a pattern of a small dot-like staining within epithelial cytoplasm during gestation and the first day postnatal, then changed to a pattern of diffuse cytoplasmic staining by the 7th postnatal day. This study concludes that 1) expression of three isoforms of NOS is present and regulated during lung development; 2) markedly increased NOS in epithelium near term supports a role for NO in mediating the pulmonary transition from fetal to neonatal life; and 3) eNOS immunohistochemistry serves as an effective marker to follow the process of pulmonary angiogenesis and suggests the concept of in situ formation of endothelial vesicles in developing mesenchyme.

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Rivalland, Gareth, Paul Mitchell, Carmel Murone, Khashayer Asadi, Adrienne L. Morey, Maud Starmans, Paul C. Boutros, et al. "Mesenchyme to epithelial transition protein expression, gene copy number and clinical outcome in a large non-small cell lung cancer surgical cohort." Translational Lung Cancer Research 8, no. 2 (April 2019): 167–75. http://dx.doi.org/10.21037/tlcr.2019.03.11.

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Jeon, Hyun Min, Su Yeon Lee, Min Kyung Ju, Hye Gyeong Park, and Ho Sung Kang. "Early Growth Response 1 Induces Epithelial-to-mesenchymal Transition via Snail." Journal of Life Science 23, no. 8 (August 30, 2013): 970–77. http://dx.doi.org/10.5352/jls.2013.23.8.970.

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Journal articles on the topic 'Epithelial mesenchyme transition'

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