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Biomarkers for epithelial-mesenchymal transitions
Open accessAbstract
Somatic cells that change from one mature phenotype to another exhibit the property of plasticity. It is increasingly clear that epithelial and endothelial cells enjoy some of this plasticity, which is easily demonstrated by studying the process of epithelial-mesenchymal transition (EMT). Published reports from the literature typically rely on ad hoc criteria for determining EMT events; consequently, there is some uncertainty as to whether the same process occurs under different experimental conditions. As we discuss in this Personal Perspective, we believe that context and various changes in plasticity biomarkers can help identify at least three types of EMT and that using a collection of criteria for EMT increases the likelihood that everyone is studying the same phenomenon - namely, the transition of epithelial and endothelial cells to a motile phenotype.
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“Moreover, proteins in the most significantly up-regulated network module (Extended Data Fig. 10d, 10f) included collagens (COL1A1 and COL3A1) and extracellular matrix glycoproteins (FN1, BGN, FBN1, and FBN2) that also are markers of EMT34, 35.”
From Proteogenomic characterization of human colon and rectal cancer (2014) · cites this paper as [35]
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“knockdown of HIF-1α inhibits or even reverses the EMT-like phenotype (103, 104).”
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“Interestingly, stimulation of LECs with recombinant TGF- 1 markedly increased the expression of putative EMT markers collagen I, N-cadherin, and FAP (73).”
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“array of genes that have been reported to be involved in cancer invasion and metastasis (18, 19).”
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aV integrins and TGF‐β‐induced EMT: a circle of regulation
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“[69, 70, 71, 72, 73] Since the deepest and most invasive areas of tumor are histologically located at the ITF, these areas are known to orchestrate the clinical behavior.”
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“of type 3 epithelial-to-mesenchymal transition [3–8];”
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“We also found higher transcript levels for SNAI2, S100A4 and VIM, which are markers of the epithelial-mesenchymal transition (28) and for the mesenchymal stem cell marker SPARC.”
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“To further characterize the EMT in C1 and C2 subgroups, several sources of positive and negative EMT markers described in relevant publications were assembled (32-34) (list given in Supplementary Table S2).”
BackgroundTransglutaminase 2: A multi-tasking protein in the complex circuitry of inflammation and cancer
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“A variety of biomarkers have been demonstrated for studies on EMT, including E-cadherin, N-cadherin, Vimentin, Snail, Zeb1, Twist and others [6].”
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“Snail1 as an EMT transcription factor coordinates the repression of epithelial phenotype and the induction of mesenchymal phenotype (24, 25).”
BackgroundDysregulation of EMT Drives the Progression to Clinically Aggressive Sarcomatoid Bladder Cancer
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“In this context, collagen type I and HSP47 expression is recently considered to be one of the useful parameters for recognizing EMT [28].”
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“Expression of transcriptional regulators such as SNAI1/2 and TWIST, followed by transcriptional switching from epithelial markers to mesenchymal ones, also has been reported.(2,11,12)”
BackgroundThe network of epithelial–mesenchymal transition: potential new targets for tumor resistance
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“To target EMT, a number of microRNAs (miRNAs) are shown to be accountable for the transition driving and reversing EMT processes (Kalluri and Weinberg 2009; Lamouille et al. 2013; Zeisberg and Neilson 2009).”
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“Some of them may potentially serve as the process markers [111].”
BackgroundMathematical Modelling of Molecular Pathways Enabling Tumour Cell Invasion and Migration
Cohen, D., Martignetti, L., Robine, S., Barillot, E., Zinovyev, A. Y., & Calzone, L. (2015) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1004571 · Cited by 141
“Gene expression of E-cadherin is inhibited by the transcription factors Snai1/2, Zeb1/2 and Twist1, while gene expression of Ncadherin (cdh2) is induced by the same transcription factors [8,10,11].”
BackgroundLi, Q., Chen, C., Kapadia, A., Zhou, Q., Harper, M. K., Schaack, J. B., & LaBarbera, D. V. (2011) · SLAS DISCOVERY · doi:10.1177/1087057110392995 · Cited by 144
Kim, W. K., Kwon, Y., Jang, M., Park, M., Kim, J., Cho, S.-Y., Jang, D. G., Lee, W.-B., Jung, S. H., Choi, H. J., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-54890-9 · Cited by 152
Vimentin expression predicts the occurrence of metastases in non small cell lung carcinomas
Dauphin, M., Barbe, C., Lemaire, S., Nawrocki‐Raby, B., Lagonotte, E., Delépine, G., Birembaut, P. L., Gilles, C., & Polette, M. (2013) · Lung Cancer · doi:10.1016/j.lungcan.2013.03.011 · Cited by 138
“Vimentin is considered as a hallmark of mesenchymal-like conversion of epithelial cells and appears to be one of the best indicators of EMT in carcinomas [3].”
BackgroundInhibiting Interactions of Lysine Demethylase LSD1 with Snail/Slug Blocks Cancer Cell Invasion
Ferrari‐Amorotti, G., Fragliasso, V., Esteki, R., Prudente, Z., Soliera, A. R., Cattelani, S., Manzotti, G., Grisendi, G., Dominici, M., Pieraccioli, M., et al. (2012) · Cancer Research · doi:10.1158/0008-5472.can-12-1739 · Cited by 139
“through which tumor cells lose homotypic adhesion, change morphology, and acquire migratory capacity (4, 5).”
Renal Endothelial Dysfunction in Diabetic Nephropathy
Cheng, H., & Harris, R. C. (2014) · Cardiovascular & Haematological Disorders - Drug Targets · doi:10.2174/1871529x14666140401110841 · Cited by 138
“EndoMT has been suggested to play an important role in organ fibrosis and cancer progression [52].”
Recurrent Oral Cancer: Current and Emerging Therapeutic Approaches
da Silva, S. D., Hier, M., Mlynarek, A., Kowalski, L. P., & Alaoui‐Jamali, M. A. (2012) · Frontiers in Pharmacology · doi:10.3389/fphar.2012.00149 · Cited by 138
“Preclinical studies also reported a significant correlation between EMT phenotype, drug resistance, and relapses (Zeisberg and Neilson, 2009) including in OCC patients (Machiels and Schmitz, 2011; Raza et al., 2011).”
BackgroundWik, E., Raeder, M. B., Krakstad, C., Trovik, J., Birkeland, E., Høivik, E. A., Mjøs, S., Werner, H. M. J., Mannelqvist, M., Stefansson, I. M., et al. (2013) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-12-3039 · Cited by 136
“EMT signature scores In the prospective validation cohort, the mRNA expression values (by qPCR) for a selection of cell adhesion markers known from the literature to be related to EMT (11, 26, 27) were assessed to calculate an mRNA signature score reflecting the EMTprocess.”
BackgroundMethodJabbari, E., Sarvestani, S. K., Daneshian, L., & Moeinzadeh, S. (2015) · PLoS ONE · doi:10.1371/journal.pone.0132377 · Cited by 133
“Other EMT markers include Snail, Slug, Twist, ZEB2, TGF-β, and vimentin (Vim) [59,60].”
BackgroundRetractedGeorgiadis, A., Tschernutter, M., Bainbridge, J. W., Balaggan, K. S., Mowat, F. M., West, E. L., Munro, P., Thrasher, A. J., Matter, K., Balda, M. S., et al. (2010) · PLoS ONE · doi:10.1371/journal.pone.0015730 · Cited by 135
“Some of the EMT markers upregulated in transformed cells are glial fibrillary acidic protein (GFAP), vimentin, cyclin D1 (cD1), alpha smooth muscle actin (a-SMA), Snail1, C-terminal binding protein 1 (CtBP1) and N-Cadherin (with corresponding loss of E-cad) [22,24,26,27, 28,29].”
BackgroundCruz-Solbes, A. S., & Youker, K. A. (2017) · Results and problems in cell differentiation · doi:10.1007/978-3-319-51436-9_13 · Cited by 139
Vered, M., Dayan, D., Yahalom, R., Dobriyan, A., Barshack, I., Bello, I. O., Kantola, S., & Salo, T. A. (2010) · International Journal of Cancer · doi:10.1002/ijc.25358 · Cited by 134
The epithelial to mesenchymal transition in pancreatic cancer: A systematic review
Beuran, M., Negoi, I., Paun, S. C., Ion, D. A., Bleoţu, C., Negoi, R. I., & Hostiuc, S. (2015) · Pancreatology · doi:10.1016/j.pan.2015.02.011 · Cited by 133
Liu, H., Korc, M., & Lin, C. (2018) · Biomaterials · doi:10.1016/j.biomaterials.2018.01.012 · Cited by 134
Alyaseer, A. A. A., de Lima, M. H. S., & Braga, T. T. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00883 · Cited by 135
“The type I EMT is present in embryogenesis implantation, during the initiation of the placenta development and organ development; the type II EMT, on the other hand, occurs during fibrotic diseases in organs such as the liver, kidney, lung, and intestine, and it is also associated with tissue regeneration and wound he…”
BackgroundRebuilding cancer metastasis in the mouse
Saxena, M. T., & Christofori, G. (2013) · Molecular Oncology · doi:10.1016/j.molonc.2013.02.009 · Cited by 139
“The hallmark properties of ametastatic cell are its ability to migrate and invade into the surrounding tissue (Zeisberg and Neilson, 2009).”
BackgroundLong non-coding RNA regulation of epithelial–mesenchymal transition in cancer metastasis
Xu, Q., Deng, F., Qin, Y., Zhao, Z., Wu, Z., Xing, Z., Ji, A., & Wang, Q. J. (2016) · Cell Death and Disease · doi:10.1038/cddis.2016.149 · Cited by 132
“Fibronectin mediates cellular interactions with the extracellular matrix and is important for migration, differentiation, growth, and cell adhesion (Figure 1).(8)”
BackgroundDirect Transcriptional Reprogramming of Adult Cells to Embryonic Nephron Progenitors
Hendry, C., Vanslambrouck, J. M., Ineson, J., Suhaimi, N., Takasato, M., Rae, F., & Little, M. H. (2013) · Journal of the American Society of Nephrology · doi:10.1681/asn.2012121143 · Cited by 134
Vázquez, F., García-Ocaña, M., Galván, J. A., García–Martínez, J., García-Pravia, C., Menéndez‐Rodríguez, P., del Rey, C. G., Barneo, L., & Toyos, J. R. D. L. (2015) · Tumor Biology · doi:10.1007/s13277-015-3295-4 · Cited by 131
“Traits associated with a type 3 EMT are the acquisition of a spindle shape, the upregulation of vimentin (VIM), and the Bcadherin switching,^ consisting in the progressive loss of E-cadherin (CDH1) and the increase in N-cadherin and OB-cadherin or cadherin-11 (CDH11) expression.”
BackgroundInfluentialSohal, S. S., Reid, D. W., Soltani, A., Ward, C., Weston, S., Muller, H. K., Wood-Baker, R. R., & Walters, E. H. (2011) · Respiratory Research · doi:10.1186/1465-9921-12-130 · Cited by 132
“Active EMT is indicated by the degradation of underlying epithelial basement membrane and transition of epithelial cells into mesenchymal cells with migratory potential, such that they move away from the epithelium in which they originated into deeper tissue [12,15].”
BackgroundInfluentialBiomarkers for EMT and MET in breast cancer: An update
Liu, F., Gu, L., Shan, B.-E., Geng, C., & Sang, M. (2016) · Oncology Letters · doi:10.3892/ol.2016.5369 · Cited by 139
“Subsequently, β -catenin translocates to the nucleus to promote the transcription of genes that induce EMT (41).”
InfluentialHan, M., Wang, Y., Liu, M., Bi, X., Bao, J., Zeng, N., Zhu, Z.-K., Mo, Z., Wu, C., & Chen, X. (2012) · Cancer Science · doi:10.1111/j.1349-7006.2012.02281.x · Cited by 131
Wilson, M. R., Reske, J. J., Holladay, J., Moldovan, G. E., Rhodes, M., Koeman, J. M., Adams, M., Johnson, B. K., Su, R., Joshi, N., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-11403-6 · Cited by 127
Regulation of the Epithelial-Mesenchymal Transition by Claudin-3 and Claudin-4
Lin, X., Shang, X., Manorek, G., & Howell, S. B. (2013) · PLoS ONE · doi:10.1371/journal.pone.0067496 · Cited by 129
“2, Goosecoid, LEF-1 and FoxC2, as well as N-cadherin, vimentin, fibronectin, miR10b, and miR21 [4,63,64].”
Activation of the Notch1/STAT3/Twist signaling axis promotes gastric cancer progression
Hsu, K., Hsieh, R., Huang, K., Li, A. F., Chi, C., Wang, T.-Y., Tseng, M.-J., Wu, K.-J., & Yeh, T.-S. (2012) · Carcinogenesis · doi:10.1093/carcin/bgs165 · Cited by 127
Organ Fibrosis and Autoimmunity: The Role of Inflammation in TGFβ-Dependent EMT
Sisto, M., Ribatti, D., & Lisi, S. (2021) · Biomolecules · doi:10.3390/biom11020310 · Cited by 130
“Recently, EMT has been identified as a new source of cells with a mesenchymal phenotype involved in the progression of fibrotic diseases [3,17,35].”
BackgroundPattabiraman, P. P., Maddala, R., & Rao, P. V. (2013) · Journal of Cellular Physiology · doi:10.1002/jcp.24524 · Cited by 125
“…in TM cells (Nakamura et al., 2002; Mettu et al., 2004; Pattabiraman and Rao, 2010; Junglas et al., 2012), were found to increase both the expression and protein levels of myofibroblast markers FSP-1, aSMA, and collagen-1A1 in HTM cells (Kalluri and Neilson, 2003; Zeisberg and Neilson, 2009).”
BackgroundEmerging roles of radioresistance in prostate cancer metastasis and radiation therapy
Chang, L., Graham, P., Hao, J., Bucci, J. A., Cozzi, P. J., Kearsley, J. H., & Li, Y. (2014) · Cancer and Metastasis Reviews · doi:10.1007/s10555-014-9493-5 · Cited by 126
Mechanical Control of Epithelial-to-Mesenchymal Transitions in Development and Cancer
Przybyla, L., Muncie, J. M., & Weaver, V. M. (2016) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-111315-125150 · Cited by 123
Trophoblast invasion: Lessons from abnormally invasive placenta (placenta accreta)
Illsley, N. P., DaSilva‐Arnold, S. C., Zamudio, S., Alvarez, M., & Al‐Khan, A. (2020) · Placenta · doi:10.1016/j.placenta.2020.01.004 · Cited by 125
“We speculate that CTB differentiation may be the molecular archetypal EMT, a “type 0” EMT, as it occurs so early in human development compared to EMT types 1–3 [44,48].”
BackgroundSeok, J. K., Lee, S. H., Kim, M. J., & Lee, Y.-M. (2014) · Nucleic Acids Research · doi:10.1093/nar/gku515 · Cited by 124
“and reversion to cancer stem cells (42).”
Wang, M., Qiu, R., Yu, S., Xu, X., Li, G., Gu, R., Tan, C., Zhu, W., & Shen, B. (2018) · International Journal of Oncology · doi:10.3892/ijo.2018.4601 · Cited by 124
“mesenchymal markers, including N‐cadherin, Vimentin and Fibronectin (53).”
CDK5 is essential for TGF-β1-induced epithelial-mesenchymal transition and breast cancer progression
Liang, Q. Y., Li, L., Zhang, J., Yang, L., Wang, L., Liu, D., Feng, J., Hou, P., Yao, R., Zhang, Y., et al. (2013) · Scientific Reports · doi:10.1038/srep02932 · Cited by 123
CHANG, L., Li, C., Lan, T., Wu, L., Yuan, Y., Liu, Q., & Liu, Z. (2015) · Molecular Medicine Reports · doi:10.3892/mmr.2015.4716 · Cited by 123
“Various biomarkers have been screened to indicate the EMT process, including the loss of E-cadherin, zona occludens-1 and cytokeratin, and the upregulation of matrix metalloproteinase, fibronectin, α -smooth muscle actin, vimentin, snail and slug (35).”
Metadata
- Authors
- Zeisberg, M., & Neilson, E. G.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Vanderbilt University (US)
- Venue
- Journal of Clinical Investigation
- Published
- 2009-06-01
- Volume
- 119
- Issue
- 6
- Pages
- 1429-1437
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC2689132
- OpenAlex
- W1996118868
- Cited by
- 2,299
- References
- 124
- Citations by year
- 2026: 50 · 2025: 79 · 2024: 127 · 2023: 113 · 2022: 146 · 2021: 148 · 2020: 180 · 2019: 163 · 2018: 170 · 2017: 189 · 2016: 153 · 2015: 162 · 2014: 162 · 2013: 149 · 2012: 109
- FWCI
- 8.93
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R03DK081687, R01DK046282, DK46282, K08DK074558, DK-081687, DK074558)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Keywords
- epithelial-mesenchymal transition, cellular plasticity, epithelial cells, endothelial cells, cell motility
- MeSH terms
- Animals, Cell Differentiation, Epithelial Cells, Fibroblasts, Humans, Neoplasms, Biomarkers, Mesenchymal Stem Cells
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