Relevant bibliographies by topics / Epithelial-mesenchymal transition / Journal articles

Journal articles on the topic 'Epithelial-mesenchymal transition'

To see the other types of publications on this topic, follow the link: Epithelial-mesenchymal transition.
Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Epithelial-mesenchymal transition.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Klymkowsky, Michael W., and Pierre Savagner. "Epithelial-Mesenchymal Transition." American Journal of Pathology 174, no. 5 (May 2009): 1588–93. http://dx.doi.org/10.2353/ajpath.2009.080545.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Han, Myung Woul, Jong Cheol Lee, Young Min Kim, Hee Jeong Cha, Jong-Lyel Roh, Seung-Ho Choi, Soon Yuhl Nam, Kyung-Ja Cho, Seong Who Kim, and Sang Yoon Kim. "Epithelial-Mesenchymal Transition." Otolaryngology–Head and Neck Surgery 152, no. 1 (November 11, 2014): 80–86. http://dx.doi.org/10.1177/0194599814556061.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Zavadil, Jiri, John Haley, Raghu Kalluri, Senthil K. Muthuswamy, and Erik Thompson. "Epithelial-Mesenchymal Transition." Cancer Research 68, no. 23 (December 1, 2008): 9574–77. http://dx.doi.org/10.1158/0008-5472.can-08-2316.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Radisky, D. C. "Epithelial-mesenchymal transition." Journal of Cell Science 118, no. 19 (September 13, 2005): 4325–26. http://dx.doi.org/10.1242/jcs.02552.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Sharma, Anil K., and Rolf D. Hubmayr. "Epithelial to mesenchymal transition." Critical Care Medicine 40, no. 2 (February 2012): 682–83. http://dx.doi.org/10.1097/ccm.0b013e318232d1a8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Luft, Friedrich C. "Targeting epithelial–mesenchymal transition." Journal of Molecular Medicine 93, no. 7 (June 14, 2015): 703–5. http://dx.doi.org/10.1007/s00109-015-1302-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Manfioletti, Guidalberto, and Monica Fedele. "Epithelial–Mesenchymal Transition (EMT)." International Journal of Molecular Sciences 24, no. 14 (July 13, 2023): 11386. http://dx.doi.org/10.3390/ijms241411386.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Shcherbakov, V., T. Ryabichenko, G. Skosyreva, and A. Trunov. "EPITHELIAL-MESENCHYMAL AND MESENCHYMAL-EPITHELIAL TRANSITION, PATHOGENESIS, REGULATION, THERAPY." Problems in oncology 64, no. 1 (January 2, 2018): 62–72. http://dx.doi.org/10.37469/0507-3758-2018-64-1-62-72.

Full text
Abstract:
The review considered the issues of epithelial-mesenchymal transition (EMT) and its role in inflammation, fibrosis, tumor growth. There were analyzed mechanisms and classification of EMT. A comparison of different forms of EMTs was performed. The important role of EMT in the formation of metastasis-initiating cells was noted. There were presented data on the role of fibroblasts in fibrosis of the lung, carcinogenesis. Stimulators and inhibitors of EMTs were summarized. There were considered intracellular paths that were associated with the development of the EMT under the influence of transforming growth factor ß1 (TGF - ß1). It also induced the development of local hypothyroidism, for easy expression of oncofetal genes, which was especially important in tumor growth. Therapy EMT was associated with blocking the actions of TGF - ß1 and was an important area in anticancer therapy.
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Thomson, Timothy M., Cristina Balcells, and Marta Cascante. "Metabolic Plasticity and Epithelial-Mesenchymal Transition." Journal of Clinical Medicine 8, no. 7 (July 3, 2019): 967. http://dx.doi.org/10.3390/jcm8070967.

Full text
Abstract:
A major transcriptional and phenotypic reprogramming event during development is the establishment of the mesodermal layer from the ectoderm through epithelial-mesenchymal transition (EMT). EMT is employed in subsequent developmental events, and also in many physiological and pathological processes, such as the dissemination of cancer cells through metastasis, as a reversible transition between epithelial and mesenchymal states. The remarkable phenotypic remodeling accompanying these transitions is driven by characteristic transcription factors whose activities and/or activation depend upon signaling cues and co-factors, including intermediary metabolites. In this review, we summarize salient metabolic features that enable or instigate these transitions, as well as adaptations undergone by cells to meet the metabolic requirements of their new states, with an emphasis on the roles played by the metabolic regulation of epigenetic modifications, notably methylation and acetylation.
APA, Harvard, Vancouver, ISO, and other styles
11

Kamlund, Sofia, Birgit Janicke, Kersti Alm, Robert L. Judson-Torres, and Stina Oredsson. "Quantifying the Rate, Degree, and Heterogeneity of Morphological Change during an Epithelial to Mesenchymal Transition Using Digital Holographic Cytometry." Applied Sciences 10, no. 14 (July 9, 2020): 4726. http://dx.doi.org/10.3390/app10144726.

Full text
Abstract:
Cells in complex organisms can transition between epithelial and mesenchymal phenotypes during both normal and malignant physiological events. These two phenotypes are not binary, but rather describe a spectrum of cell states along an axis. Mammalian cells can undergo dynamic and heterogenous bidirectional interconversions along the epithelial–mesenchymal phenotypic (EMP) spectrum, and such transitions are marked by morphological change. Here, we exploit digital holographic cytometry (DHC) to develop a tractable method for monitoring the degree, kinetics, and heterogeneity of epithelial and mesenchymal phenotypes in adherent mammalian cell populations. First, we demonstrate that the epithelial and mesenchymal states of the same cell line present distinct DHC-derived morphological features. Second, we identify quantitative changes in these features that occur hours after induction of the epithelial to mesenchymal transition (EMT). We apply this approach to achieve label-free tracking of the degree and the rate of EMP transitions. We conclude that DHC is an efficient method to investigate morphological changes during transitions between epithelial and mesenchymal states.
APA, Harvard, Vancouver, ISO, and other styles
12

Ishida, Mitsuaki, Akie Takebayashi, Fuminori Kimura, Akiko Nakamura, Jun Kitazawa, Aina Morimune, Tetsuro Hanada, Koji Tsuta, and Takashi Murakami. "Induction of the epithelial-mesenchymal transition in the endometrium by chronic endometritis in infertile patients." PLOS ONE 16, no. 4 (April 7, 2021): e0249775. http://dx.doi.org/10.1371/journal.pone.0249775.

Full text
Abstract:
Background The purpose of the present study was to evaluate the relationship between chronic endometritis and the epithelial-mesenchymal transition in the endometrium of infertile patients in the implantation phase. Methods Endometrial biopsy specimens from 66 infertility patients were analyzed. The presence of chronic endometritis was investigated by immunostaining for CD138. Immunohistochemical staining for E-cadherin, N-cadherin, Slug, and Snail was performed, and the expression profiles were statistically analyzed according to the presence of chronic endometritis. When the loss of E-cadherin expression and/or the positive expression of N-cadherin was detected, the specimen was considered epithelial-mesenchymal transition-positive. Epithelial-mesenchymal transition-positive cases were also statistically analyzed according to the presence of chronic endometritis. The characteristics of the patients in the epithelial-mesenchymal transition-positive and epithelial-mesenchymal transition-negative groups were compared. The association between variables, including age, body mass index, gravidity, parity, and each causative factor of infertility and epithelial-mesenchymal transition positivity was analyzed. Results The rates of the loss of E-cadherin expression, the gain of N-cadherin and epithelial-mesenchymal transition positivity were significantly higher in chronic endometritis patients. The expression of Slug, cytoplasmic Snail, and nuclear Snail was also detected at significantly higher rates in chronic endometritis patients. Chronic endometritis were related to the epithelial-mesenchymal transition. Conclusion The epithelial-mesenchymal transition was frequently detected in the endometrium in infertile patients with chronic endometritis. Since the epithelial-mesenchymal transition is associated with chronic endometritis, the epithelial-mesenchymal transition appears to be involved in the alteration of mechanisms of implantation.
APA, Harvard, Vancouver, ISO, and other styles
13

Manfioletti, Guidalberto, and Monica Fedele. "Epithelial–Mesenchymal Transition (EMT) 2021." International Journal of Molecular Sciences 23, no. 10 (May 23, 2022): 5848. http://dx.doi.org/10.3390/ijms23105848.

Full text
APA, Harvard, Vancouver, ISO, and other styles
14

Mitchell, Brendon, Jagdish K. Dhingra, and Meera Mahalingam. "BRAF and Epithelial-Mesenchymal Transition." Advances In Anatomic Pathology 23, no. 4 (July 2016): 244–71. http://dx.doi.org/10.1097/pap.0000000000000113.

Full text
APA, Harvard, Vancouver, ISO, and other styles
15

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
16

Eger, Andreas, and Wolfgang Mikulits. "Models of epithelial–mesenchymal transition." Drug Discovery Today: Disease Models 2, no. 1 (March 2005): 57–63. http://dx.doi.org/10.1016/j.ddmod.2005.04.001.

Full text
APA, Harvard, Vancouver, ISO, and other styles
17

Quarta, S., L. Vidalino, C. Turato, M. G. Ruvoletto, F. Calabrese, G. Fassina, A. Gatta, and P. Pontisso. "SERPINB3 induces epithelial mesenchymal transition." Digestive and Liver Disease 41, no. 5 (May 2009): A1—A2. http://dx.doi.org/10.1016/j.dld.2009.02.012.

Full text
APA, Harvard, Vancouver, ISO, and other styles
18

Sleeman, Jonathan P., and Jean Paul Thiery. "SnapShot: The Epithelial-Mesenchymal Transition." Cell 145, no. 1 (April 2011): 162–162. http://dx.doi.org/10.1016/j.cell.2011.03.029.

Full text
APA, Harvard, Vancouver, ISO, and other styles
19

Moustakas, Aristidis, and Antonio Garcia de Herreros. "Epithelial-mesenchymal transition in cancer." Molecular Oncology 11, no. 7 (July 2017): 715–17. http://dx.doi.org/10.1002/1878-0261.12094.

Full text
APA, Harvard, Vancouver, ISO, and other styles
20

Quarta, Santina, Laura Vidalino, Cristian Turato, Mariagrazia Ruvoletto, Fiorella Calabrese, Marialuisa Valente, Stefania Cannito, et al. "SERPINB3 induces epithelial-mesenchymal transition." Journal of Pathology 221, no. 3 (March 12, 2010): 343–56. http://dx.doi.org/10.1002/path.2708.

Full text
APA, Harvard, Vancouver, ISO, and other styles
21

Deng, Junjian, and Ximing Xu. "Epithelial-mesenchymal transition and cancermetastasis." Chinese-German Journal of Clinical Oncology 10, no. 3 (March 2011): 125–33. http://dx.doi.org/10.1007/s10330-011-0740-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
22

Shevlyuk, N. N. "Epithelial-mesenchymal transition: the history of the concept, debatable issues." Journal of Anatomy and Histopathology 12, no. 2 (July 9, 2023): 90–98. http://dx.doi.org/10.18499/2225-7357-2023-12-2-90-98.

Full text
Abstract:
The paper discusses diverse aspects of the concept of epithelial-mesenchymal transition and compares the basics of this concept with the classical concepts of tissue biology. The idea of the epithelial-mesenchymal transition was first suggested by Elizabeth Hay (1927–2007) in 1968 based on the analysis of tridermogenesis in the development and growth of the avian embryo. In the late 80s – early 90s of the twentieth century, the concept of epithelial–mesenchymal transition won supporters-pathomorphologists in our country who applied the concept to explain mechanisms of multiple pathological processes. The controversial issue arises: to which extent the concept of epithelial-mesenchymal transition is validated. It should be noted that a number of its basic principles are open to question. Thus, it is hardly correct to consider the cells of the ectoderma as epithelial cells, since they do not express immunohistochemical markers of epithelial tissue cells. That is, cells with a true epithelial phenotype are not yet represented at this stage of embryogenesis. It should also be taken into account that all evidence for the epithelial-mesenchymal transition is based on indirect immunocytochemical findings (decreased expression of epithelial markers, increased expression of markers of mesenchymal tissue genesis). Moreover, saying about the “epithelial-mesenchymal transition” specialists mean cell populations and not specific cells, which is hardly the same. All the above allows arguing the existence of the epithelial-mesenchymal transition; this issue needs additional research and more fact-based support.
APA, Harvard, Vancouver, ISO, and other styles
23

Bhatia, Monkman, Blick, Pinto, Waltham, Nagaraj, and Thompson. "Interrogation of Phenotypic Plasticity between Epithelial and Mesenchymal States in Breast Cancer." Journal of Clinical Medicine 8, no. 6 (June 21, 2019): 893. http://dx.doi.org/10.3390/jcm8060893.

Full text
Abstract:
Dynamic interconversions between transitional epithelial and mesenchymal states underpin the epithelial mesenchymal plasticity (EMP) seen in some carcinoma cell systems. We have delineated epithelial and mesenchymal subpopulations existing within the PMC42-LA breast cancer cell line by their EpCAM expression. These purified but phenotypically plastic states, EpCAMHigh (epithelial) and EpCAMLow (mesenchymal), have the ability to regain the phenotypic equilibrium of the parental population (i.e., 80% epithelial and 20% mesenchymal) over time, although the rate of reversion in the mesenchymal direction (epithelial-mesenchymal transition; EMT) is higher than that in the epithelial direction (mesenchymal-epithelial transition; MET). Single-cell clonal propagation was implemented to delineate the molecular and cellular features of this intrinsic heterogeneity with respect to EMP flux. The dynamics of the phenotypic proportions of epithelial and mesenchymal states in single-cell generated clones revealed clonal diversity and intrinsic plasticity. Single cell-derived clonal progenies displayed differences in their functional attributes of proliferation, stemness marker (CD44/CD24), migration, invasion and chemo-sensitivity. Interrogation of genomic copy number variations (CNV) with whole exome sequencing (WES) in the context of chromosome count from metaphase spread indicated that chromosomal instability was not influential in driving intrinsic phenotypic plasticity. Overall, these findings reveal the stochastic nature of both the epithelial and mesenchymal subpopulations, and the single cell-derived clones for differential functional attributes.
APA, Harvard, Vancouver, ISO, and other styles
24

Stunf Pukl, Spela. "MicroRNA of Epithelial to Mesenchymal Transition in Fuchs’ Endothelial Corneal Dystrophy." Genes 13, no. 10 (September 23, 2022): 1711. http://dx.doi.org/10.3390/genes13101711.

Full text
Abstract:
Aim: a review of miRNA expression connected to epithelial mesenchymal transition studies in Fuchs’ endothelial corneal dystrophy (FECD). Methods: literature search strategy—PubMed central database, using “miRNA” or “microRNA“ and “epithelial mesenchymal transition” or “EMT“ and “Fuchs’ endothelial corneal dystrophy” or “FECD” as keywords. Experimental or clinical studies on humans published in English regarding miRNA profiles of epithelial mesenchymal transition in Fuchs’ endothelial corneal dystrophy published between 2009 and 2022 were included. Conclusion: The publications regarding the miRNA profiles of epithelial mesenchymal transition in Fuchs’ endothelial corneal dystrophy are scarce but provide some valuable information about the potential biomarkers differentiating aging changes from early disease stages characterized by epithelial mesenchymal transition. In the corneal tissue of FECD patients, miRNA-184 seed-region mutation as well as unidirectional downregulation of total miRNA expression led by the miRNA-29 were demonstrated. For early diagnostics the miRNA of epithelial mesenchymal transition in aqueous humor should be analyzed and used as biomarkers.
APA, Harvard, Vancouver, ISO, and other styles
25

Kovacic, Jason C., Nadia Mercader, Miguel Torres, Manfred Boehm, and Valentin Fuster. "Epithelial-to-Mesenchymal and Endothelial-to-Mesenchymal Transition." Circulation 125, no. 14 (April 10, 2012): 1795–808. http://dx.doi.org/10.1161/circulationaha.111.040352.

Full text
APA, Harvard, Vancouver, ISO, and other styles
26

Jayan, Lekshmy, R. Bharanidharan, and Ramya Ramdas. "Epithelial-Mesenchymal Interactions in Embryogenesis and Head and Neck Tumors." Journal of Surgical Case Reports and Images 2, no. 1 (December 18, 2019): 01–08. http://dx.doi.org/10.31579/2690-1897/007.

Full text
Abstract:
Epithelial mesenchymal interactions are one of the most important process taking place in the body. It is an indispensable mechanism that mediates the development of numerous organs and organ systems especially tooth, salivary gland etc. It has been long implicated in the causation of numerous pathogenic processes especially cancer. The mechanism of epithelial mesenchymal interactions are a forerunner for epithelial mesenchymal transition, which is an important pathological process in the development of cancer. In this review, we have highlighted the role of epithelial mesenchymal interactions in normal embryogenesis as well in numerous pathological conditions.
APA, Harvard, Vancouver, ISO, and other styles
27

Jayan, Lekshmy. "Epithelial-Mesenchymal Interactions in Embryogenesis and Head and Neck Tumors." Journal of Surgical Case Reports and Images 1, no. 2 (November 29, 2019): 01–08. http://dx.doi.org/10.31579/jscr/2019/007.

Full text
Abstract:
Epithelial mesenchymal interactions are one of the most important process taking place in the body. It is an indispensable mechanism that mediates the development of numerous organs and organ systems especially tooth, salivary gland etc. It has been long implicated in the causation of numerous pathogenic processes especially cancer. The mechanism of epithelial mesenchymal interactions are a forerunner for epithelial mesenchymal transition, which is an important pathological process in the development of cancer. In this review, we have highlighted the role of epithelial mesenchymal interactions in normal embryogenesis as well in numerous pathological conditions.
APA, Harvard, Vancouver, ISO, and other styles
28

Kushwaha, Sandhya, Deepti Jindal, Sonia Joshi, Ashwini P., and Poorva Tiwari. "Exploring the Role of Cadherins in Epithelial–Mesenchymal Transition and Mesenchymal–Epithelial Transition-Associated Tumorigenesis." Dental Journal of Advance Studies 6, no. 02/03 (October 26, 2018): 045–52. http://dx.doi.org/10.1055/s-0038-1673588.

Full text
Abstract:
AbstractThe malignant tumors develop when tumor cells overcome the cell–cell adhesion and invade the surrounding tissue. The epithelium consists of E-cadherin as the main adhesion molecule, which is mainly implicated in the carcinogenesis as it is frequently lost in the human epithelial tumors. Epithelial–mesenchymal transition (EMT) and its reverse mesenchymal–epithelial transition (MET) have been suggested to play crucial roles in metastatic dissemination of carcinomas. E-cadherin loss may promote invasion, and re-expression may facilitate cell survival within metastatic deposits. The mechanisms underlying such plasticity are unclear. Here, we summarize the role of cadherins in EMT- and MET-associated tumorigenesis by accumulating the experimental evidences that directly supports it.
APA, Harvard, Vancouver, ISO, and other styles
29

Zhao, Min, Lin Ang, Jin Huang, and Jin Wang. "MicroRNAs regulate the epithelial–mesenchymal transition and influence breast cancer invasion and metastasis." Tumor Biology 39, no. 2 (February 2017): 101042831769168. http://dx.doi.org/10.1177/1010428317691682.

Full text
Abstract:
MicroRNAs are small RNA molecules that play a major role in the post-transcriptional regulation of genes and influence the development, differentiation, proliferation, and apoptosis of cells and the development and progression of tumors. The epithelial–mesenchymal transition is a process by which epithelial cells morphologically transform into cells with a mesenchymal phenotype. The epithelial–mesenchymal transition plays a highly important role in tumor invasion and metastasis. Increasing evidence indicates that microRNAs are tightly associated with epithelial–mesenchymal transition regulation in tumor cells. In breast cancer, various microRNA molecules have been identified as epithelial–mesenchymal transition inducers or inhibitors, which, through different mechanisms and signaling pathways, participate in the regulation of breast cancer invasion and metastasis among various biological behaviors. The epithelial–mesenchymal transition–related microRNAs in breast cancer provide valuable molecules for researching cell invasion and metastasis, and they also provide candidate targets that may be significant for the targeted therapy of breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
30

Varankar, Sagar S., Madhuri More, Ancy Abraham, Kshama Pansare, Brijesh Kumar, Nivedhitha J. Narayanan, Mohit Kumar Jolly, Avinash M. Mali, and Sharmila A. Bapat. "Functional balance between Tcf21–Slug defines cellular plasticity and migratory modalities in high grade serous ovarian cancer cell lines." Carcinogenesis 41, no. 4 (June 25, 2019): 515–26. http://dx.doi.org/10.1093/carcin/bgz119.

Full text
Abstract:
Abstract Cellular plasticity and transitional phenotypes add to complexities of cancer metastasis that can be initiated by single cell epithelial to mesenchymal transition (EMT) or cooperative cell migration (CCM). Our study identifies novel regulatory cross-talks between Tcf21 and Slug in mediating phenotypic and migration plasticity in high-grade serous ovarian adenocarcinoma (HGSC). Differential expression and subcellular localization associate Tcf21, Slug with epithelial, mesenchymal phenotypes, respectively; however, gene manipulation approaches identify their association with additional intermediate phenotypic states, implying the existence of a multistep epithelial-mesenchymal transition program. Live imaging further associated distinct migratory modalities with the Tcf21/Slug status of cell systems and discerned proliferative/passive CCM, active CCM and EMT modes of migration. Tcf21–Slug balance identified across a phenotypic spectrum in HGSC cell lines, associated with microenvironment-induced transitions and the emergence of an epithelial phenotype following drug exposure. Phenotypic transitions and associated functionalities following drug exposure were affirmed to ensue from occupancy of Slug promoter E-box sequences by Tcf21. Our study effectively provides a framework for understanding the relevance of ovarian cancer plasticity as a function of two transcription factors.
APA, Harvard, Vancouver, ISO, and other styles
31

Enderle-Ammour, Kathrin, Moritz Bader, Theresa Dorothee Ahrens, Kai Franke, Sylvia Timme, Agnes Csanadi, Jens Hoeppner, et al. "Form follows function: Morphological and immunohistological insights into epithelial–mesenchymal transition characteristics of tumor buds." Tumor Biology 39, no. 5 (May 2017): 101042831770550. http://dx.doi.org/10.1177/1010428317705501.

Full text
Abstract:
In cancer biology, the architectural concept “form follows function” is reflected by cell morphology, migration, and epithelial–mesenchymal transition protein pattern. In vivo, features of epithelial–mesenchymal transition have been associated with tumor budding, which correlates significantly with patient outcome. Hereby, the majority of tumor buds are not truly detached but still connected to a major tumor mass. For detailed insights into the different tumor bud types and the process of tumor budding, we quantified tumor cells according to histomorphological and immunohistological epithelial–mesenchymal transition characteristics. Three-dimensional reconstruction from adenocarcinomas (pancreatic, colorectal, lung, and ductal breast cancers) was performed as published. Tumor cell morphology and epithelial–mesenchymal transition characteristics (represented by zinc finger E-box-binding homeobox 1 and E-Cadherin) were analyzed qualitatively and quantitatively in a three-dimensional context. Tumor buds were classified into main tumor mass, connected tumor bud, and isolated tumor bud. Cell morphology and epithelial–mesenchymal transition marker expression were assessed for each tumor cell. Epithelial–mesenchymal transition characteristics between isolated tumor bud and connected tumor bud demonstrated no significant differences or trends. Tumor cell count correlated significantly with epithelial–mesenchymal transition and histomorphological characteristics. Regression curve analysis revealed initially a loss of membranous E-Cadherin, followed by expression of cytoplasmic E-Cadherin and subsequent expression of nuclear zinc finger E-box-binding homeobox 1. Morphologic changes followed later in this sequence. Our data demonstrate that connected and isolated tumor buds are equal concerning immunohistochemical epithelial–mesenchymal transition characteristics and histomorphology. Our data also give an insight in the process of tumor budding. While there is a notion that the epithelial–mesenchymal transition zinc finger E-box-binding homeobox 1–E-Cadherin cascade is initiated by zinc finger E-box-binding homeobox 1, our results are contrary and outline other possible pathways influencing the regulation of E-Cadherin.
APA, Harvard, Vancouver, ISO, and other styles
32

Font-Clos, Francesc, Stefano Zapperi, and Caterina A. M. La Porta. "Topography of epithelial–mesenchymal plasticity." Proceedings of the National Academy of Sciences 115, no. 23 (May 21, 2018): 5902–7. http://dx.doi.org/10.1073/pnas.1722609115.

Full text
Abstract:
The transition between epithelial and mesenchymal states has fundamental importance for embryonic development, stem cell reprogramming, and cancer progression. Here, we construct a topographic map underlying epithelial–mesenchymal transitions using a combination of numerical simulations of a Boolean network model and the analysis of bulk and single-cell gene expression data. The map reveals a multitude of metastable hybrid phenotypic states, separating stable epithelial and mesenchymal states, and is reminiscent of the free energy measured in glassy materials and disordered solids. Our work not only elucidates the nature of hybrid mesenchymal/epithelial states but also provides a general strategy to construct a topographic representation of phenotypic plasticity from gene expression data using statistical physics methods.
APA, Harvard, Vancouver, ISO, and other styles
33

Desai, Krisha, Radhika Aiyappa, Jyothi S. Prabhu, Madhumathy G. Nair, Patrick Varun Lawrence, Aruna Korlimarla, Anupama CE, et al. "HR+HER2− breast cancers with growth factor receptor–mediated EMT have a poor prognosis and lapatinib downregulates EMT in MCF-7 cells." Tumor Biology 39, no. 3 (March 2017): 101042831769502. http://dx.doi.org/10.1177/1010428317695028.

Full text
Abstract:
Despite an overall good prognosis, a significant proportion of patients with hormone receptor positive human epidermal growth factor receptor 2 negative breast cancers develop distant metastases. The metastatic potential of epithelial cells is known to be regulated by tumor–stromal interaction and mediated by epithelial-to-mesenchymal transition. Hormone receptor positive human epidermal growth factor receptor 2 negative tumors were used to estimate markers of epithelial-to-mesenchymal transition, and the luminal breast cancer cell line MCF-7 was used to examine the interactions between integrins and growth factor receptors in causation of epithelial-to-mesenchymal transition. A total of 140 primary tumors were sub-divided into groups enriched for the markers of epithelial-to-mesenchymal transition (snail family transcriptional repressor 2 and integrin β6) versus those with low levels. Within the epithelial-to-mesenchymal transition+ tumors, there was a positive correlation between the transcripts of integrin β6 and growth factor receptors—human epidermal growth factor receptor 2 and epidermal growth factor receptor. In tumors enriched for epithelial-to-mesenchymal transition markers, patients with tumors with the highest quartile of growth factor receptor transcripts had a shorter disease-free survival compared to patients with low growth factor receptor expression by Kaplan–Meier analysis (log rank, p = 0.03). Epithelial-to-mesenchymal transition was induced in MCF-7 cells by treatment with transforming growth factor beta 1 and confirmed by upregulation of SNAI1 and SNAI2 transcripts, increase of vimentin and integrin β6 protein, and repression of E-cadherin. Treatment of these cells with the dual-specificity tyrosine-kinase inhibitor lapatinib led to downregulation of epithelial-to-mesenchymal transition as indicated by lower levels of SNAI1 and SNAI2 transcripts, integrin αvβ6, and matrix metalloproteinase 9 protein. The results suggest that synergistic interactions between growth factor receptors and integrin β6 could mediate epithelial-to-mesenchymal transition and migration in a subset of luminal breast cancers and lapatinib might be effective in disrupting this interaction.
APA, Harvard, Vancouver, ISO, and other styles
34

Kucuksayan, Hakan, and Hakan Akca. "The crosstalk between p38 and Akt signaling pathways orchestrates EMT by regulating SATB2 expression in NSCLC cells." Tumor Biology 39, no. 9 (September 2017): 101042831770621. http://dx.doi.org/10.1177/1010428317706212.

Full text
Abstract:
Epithelial–mesenchymal transition is a crucial event for metastasis and could be mediated by several pathways such as phosphoinositide 3-kinase/Akt, mitogen-activated protein kinases, as well as many epigenetic regulators. Special AT-rich sequence-binding protein 2 is an epigenetic regulator involved in epithelial–mesenchymal transition and osteoblastic differentiation. It has been reported that the crosstalk between several pathways is responsible for the regulation of epithelial–mesenchymal transition in cancer cells. However, crosstalks between p38 and Akt pathways involved in epithelial–mesenchymal transition are still unknown. We recently reported that there is a crosstalk between p38 and Akt pathways in non-small-cell lung carcinoma cells, and this crosstalk is associated with E-cadherin and special AT-rich sequence-binding protein 2 expressions. Therefore, we aimed to determine whether this crosstalk has a mediator role in the regulation of epithelial–mesenchymal transition in non-small-cell lung carcinoma. Our results showed that inhibition of p38 leads to the disruption of this crosstalk via decreased expression of phosphatase and tensin homolog (PTEN) and subsequently increased activation of Akt in non-small-cell lung carcinoma cells. Then, we found that p38 inhibition upregulated special AT-rich sequence-binding protein 2 expression and reversed epithelial–mesenchymal transition in non-small-cell lung carcinoma cells. Furthermore, special AT-rich sequence-binding protein 2 knockdown abolished the effect of p38 inhibition on epithelial–mesenchymal transition in non-small-cell lung carcinoma cells. In conclusion, our results strongly indicate that the crosstalk between p38 and Akt pathways can determine special AT-rich sequence-binding protein 2 expression and epithelial character of non-small-cell lung carcinoma cells, and special AT-rich sequence-binding protein 2 is a critical epigenetic regulator for epithelial–mesenchymal transition mediated by p38 pathway in non-small-cell lung carcinoma. Our findings will contribute to illuminate the molecular mechanisms of the epithelial–mesenchymal transition process that has a critical significance for lung cancer metastasis.
APA, Harvard, Vancouver, ISO, and other styles
35

Zhuravel, B. V. "EPITHELIAL-MESENCHYMAL TRANSITION IN MELANOMA PROGRESSION: THE CONTRIBUTION OF ADAPTOR PROTEIN RUK/CIN85." Biotechnologia Acta 15, no. 2 (April 2022): 74–75. http://dx.doi.org/10.15407/biotech15.02.074.

Full text
Abstract:
The purpose of this study was to test the hypothesis that Ruk/CIN85 overexpression/knockdown in melanoma cells may be involved in the regulation of EMT. Materials and methods. The mouse melanoma cell line B16-F10 and its sublines with up-/down-regulation of Ruk/CIN85 (generated early using lentiviral technology) were used as a model for research. Melanoma cells were cultured in the complete RPMI 1610 medium under standard conditions. Proliferative activity of the cells was estimated using the MTT-test, and cell migratory potential was studied by the wound-healing assay. The data obtained were analyzed with parametric Student`s t-test. Results were expressed as mean ± SEM and significance was set at P<0.05. Results and Discussion. Cutaneous melanoma genesis is a multi-step process initiated by the transformation of a normal melanocyte following an oncogenic insult. Due to the transcriptome and metabolome reprogramming in the course of EMT, transformed melanoma cells change their phenotype and acquire increased proliferative rate, cell motility, invasiveness, and metastatic potential. According to the data obtained, overexpression of Ruk/CIN85 in B16 mouse melanoma cells (subclones Up7 and Up21) led to an increase in their proliferative activity by 1,6 and 1.8 times, respectively, at 24th hour in comparison with control Mock cells . At the 48th hour, when the cells reached confluence, the cell viability of subclones did not differ from the control ones. No statistically significant changes in the proliferative activity of B16 cells with suppressed expression of the adaptor protein (subclone Down) were found. In accordance with previous data, B16 cells overexpressing Ruk/CIN85 were characterized by strongly increased motility rate (more than twofold for both Up7 and Up21 subclones compared to control Mock cells). At the same time, knockdown of Ruk/CIN85 in B16 cells resulted in a decrease in their migratory activity by about 30%. Conclusions. All findings obtained demonstrated that the malignancy traits of melanoma B16 cells are inversely modulated upon up- and down-changes in adaptor protein Ruk/CIN85 expression levels suggesting its possible role in the control of EMT.
APA, Harvard, Vancouver, ISO, and other styles
36

Kim, Young-jin, In-Soo Choi, Hae-Mi Kang, Odgerel Zunduijamts, In-Ryoung Kim, and Bong-Soo Park. "HS-1200 Induces Apoptosis and Inhibits Epithelial-Mesenchymal Transition in Oral Squamous Carcinoma." Korean Society of Oral Health Science 10, no. 4 (December 31, 2022): 96–103. http://dx.doi.org/10.33615/jkohs.2022.10.4.96.

Full text
Abstract:
Objectives: HS-1200 is a synthetic derivative of bile acid that has been proven to induce apoptosis in various types of cancer cells. However, whether HS-1200 inhibits metastasis in oral cancer has not yet been determined. Therefore, this study aims to evaluate the anti-cancer effect of HS-1200 through the inhibition of EMT in human oral squamous cell carcinoma (OSCC). Methods: The cytotoxicity effect of HS-1200 was assessed using an MTT assay. Furthermore, the cell migration and invasion ratios were obtained using a wound-healing assay and a transwell migration assay. The expressions of protein and mRNA levels were measured using a western blot analysis and real-time PCR. Results: HS-1200 was observed to inhibit the metastasis of cancer cells by regulating EMT in SCC-25 and HSC-3 cells. Conclusions: HS-1200 exhibits considerable potential as a treatment for OSCC.
APA, Harvard, Vancouver, ISO, and other styles
37

Dong, Feng, Tingting Liu, Hao Jin, and Wenbo Wang. "Chimaphilin inhibits human osteosarcoma cell invasion and metastasis through suppressing the TGF-β1-induced epithelial-to-mesenchymal transition markers via PI-3K/Akt, ERK1/2, and Smad signaling pathways." Canadian Journal of Physiology and Pharmacology 96, no. 1 (January 2018): 1–7. http://dx.doi.org/10.1139/cjpp-2016-0522.

Full text
Abstract:
Epithelial-to-mesenchymal transition is a cellular process associated with cancer invasion and metastasis. However, the antimetastatic effects of chimaphilin remain elusive. In this study, we attempted to investigate the potential use of chimaphilin as an inhibitor of TGF-β1-induced epithelial-to-mesenchymal transition in U2OS cells. We found that TGF-β1 induced epithelial-to-mesenchymal transition to promote U2OS cell invasion and metastasis. Western blotting demonstrated that chimaphilin inhibited U2OS cell invasion and migration, increased the expression of the epithelial phenotype marker E-cadherin, repressed the expression of the mesenchymal phenotype marker vimentin, as well as decreased the level of epithelial-to-mesenchymal-inducing transcription factors Snail1 and Slug during the initiation of TGF-β1-induced epithelial-to-mesenchymal transition. In this study, we revealed that chimaphilin up-regulated the E-cadherin expression level and inhibited the production of vimentin, Snail1, and Slug in TGF-β1-induced U2OS cells by blocking PI-3K/Akt and ERK 1/2 signaling pathway. Additionally, the TGF-β1-mediated phosphorylated levels of Smad2/3 were inhibited by chimaphilin pretreatment. Above all, we conclude that chimaphilin represents an effective inhibitor of the metastatic potential of U2OS cells through suppression of TGF-β1-induced epithelial-to-mesenchymal transition.
APA, Harvard, Vancouver, ISO, and other styles
38

Guerra, A., D. J. Rodriguez, S. Montero, J. A. Betancourt-Mar, R. R. Martin, E. Silva, M. Bizzarri, G. Cocho, R. Mansilla, and J. M. Nieto-Villar. "Phase transitions in tumor growth VI: Epithelial–Mesenchymal transition." Physica A: Statistical Mechanics and its Applications 499 (June 2018): 208–15. http://dx.doi.org/10.1016/j.physa.2018.01.040.

Full text
APA, Harvard, Vancouver, ISO, and other styles
39

Maier, Harald J., Thomas Wirth, and Hartmut Beug. "Epithelial-Mesenchymal Transition in Pancreatic Carcinoma." Cancers 2, no. 4 (December 9, 2010): 2058–83. http://dx.doi.org/10.3390/cancers2042058.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Hashem, Hala. "Epithelial Mesenchymal Transition and Tissue Healing." Journal of Medical Histology 2, no. 2 (December 1, 2019): 81–102. http://dx.doi.org/10.21608/jmh.2019.7401.1046.

Full text
APA, Harvard, Vancouver, ISO, and other styles
41

Menju, Toshi, and Hiroshi Date. "Lung cancer and epithelial-mesenchymal transition." General Thoracic and Cardiovascular Surgery 69, no. 5 (March 22, 2021): 781–89. http://dx.doi.org/10.1007/s11748-021-01595-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

van Zijl, Franziska, Gudrun Zulehner, Michaela Petz, Doris Schneller, Christoph Kornauth, Mara Hau, Georg Machat, Markus Grubinger, Heidemarie Huber, and Wolfgang Mikulits. "Epithelial–mesenchymal transition in hepatocellular carcinoma." Future Oncology 5, no. 8 (October 2009): 1169–79. http://dx.doi.org/10.2217/fon.09.91.

Full text
APA, Harvard, Vancouver, ISO, and other styles
43

Broster, Seth A., and Natasha Kyprianou. "Epithelial–mesenchymal transition in prostatic disease." Future Oncology 11, no. 23 (December 2015): 3197–206. http://dx.doi.org/10.2217/fon.15.253.

Full text
APA, Harvard, Vancouver, ISO, and other styles
44

ZHAO, YA-LEI, RONG-TAO ZHU, and YU-LING SUN. "Epithelial-mesenchymal transition in liver fibrosis." Biomedical Reports 4, no. 3 (January 25, 2016): 269–74. http://dx.doi.org/10.3892/br.2016.578.

Full text
APA, Harvard, Vancouver, ISO, and other styles
45

Kogan, Samuel. "The Mesenchymal-Epithelial Transition and Metaplasia." Journal of Undergraduate Life Sciences 16, no. 1 (July 8, 2022): 4. http://dx.doi.org/10.33137/juls.v16i1.38941.

Full text
APA, Harvard, Vancouver, ISO, and other styles
46

Wu, Yanyuan, Marianna Sarkissyan, and Jaydutt Vadgama. "Epithelial-Mesenchymal Transition and Breast Cancer." Journal of Clinical Medicine 5, no. 2 (January 26, 2016): 13. http://dx.doi.org/10.3390/jcm5020013.

Full text
APA, Harvard, Vancouver, ISO, and other styles
47

Son, Hwa-Jin, and Aree Moon. "Epithelial-mesenchymal Transition and Cell Invasion." Toxicological Research 26, no. 4 (December 1, 2010): 245–52. http://dx.doi.org/10.5487/tr.2010.26.4.245.

Full text
APA, Harvard, Vancouver, ISO, and other styles
48

Venkov, Christo, David Plieth, Terri Ni, Amitava Karmaker, Aihua Bian, Alfred L. George, and Eric G. Neilson. "Transcriptional Networks in Epithelial-Mesenchymal Transition." PLoS ONE 6, no. 9 (September 30, 2011): e25354. http://dx.doi.org/10.1371/journal.pone.0025354.

Full text
APA, Harvard, Vancouver, ISO, and other styles
49

Zhao, Li-Jin, and Fang Wang. "Epithelial-to-mesenchymal transition and hepatolithiasis." World Chinese Journal of Digestology 24, no. 8 (2016): 1153. http://dx.doi.org/10.11569/wcjd.v24.i8.1153.

Full text
APA, Harvard, Vancouver, ISO, and other styles
50

Baba, Hideo, Hirohisa Okabe, Kosuke Mima, Seiya Saito, Hiromitsu Hayashi, Katsunori Imai, Hidetoshi Nitta, et al. "Epithelial-mesenchymal transition in gastroenterological cancer." Journal of Cancer Metastasis and Treatment 1, no. 3 (2015): 183. http://dx.doi.org/10.4103/2394-4722.165118.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Epithelial-mesenchymal transition' for other source types:
Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography