The DOI matches its Crossref record; 124 of the 124 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
The basics of epithelial-mesenchymal transition
Kalluri, R., & Weinberg, R. A. (2009) · Journal of Clinical Investigation · doi:10.1172/jci39104 · Cited by 10,196
The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells
Mani, S. A., Guo, W., Liao, M.-J., Eaton, E. N., Ayyanan, A., Zhou, A. Y., Brooks, M. W., Reinhard, F., Zhang, C. C., Shipitsin, M. V., et al. (2008) · Cell · doi:10.1016/j.cell.2008.03.027 · Cited by 8,839
Kalluri, R., & Zeisberg, M. (2006) · Nature Reviews Cancer · doi:10.1038/nrc1877 · Cited by 4,538
Self-citationTumors: Wounds That Do Not Heal
Flier, J. S., Underhill, L. H., & Dvorak, H. F. (1986) · New England Journal of Medicine · doi:10.1056/nejm198612253152606 · Cited by 4,391
Complex networks orchestrate epithelial–mesenchymal transitions
Thiery, J. P., & Sleeman, J. P. (2006) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1835 · Cited by 3,947
Twist, a Master Regulator of Morphogenesis, Plays an Essential Role in Tumor Metastasis
Yang, J., Mani, S. A., Donaher, J. L., Ramaswamy, S., Itzykson, R., Côme, C., Savagner, P., Gitelman, I., Richardson, A. L., & Weinberg, R. A. (2004) · Cell · doi:10.1016/j.cell.2004.06.006 · Cited by 3,917
Gregory, P. A., Bert, A. G., Paterson, E. L., Barry, S. C., Tsykin, A., Farshid, G., Vadas, M. A., Khew‐Goodall, Y., & Goodall, G. J. (2008) · Nature Cell Biology · doi:10.1038/ncb1722 · Cited by 3,852
Epithelial-Mesenchymal Transition: At the Crossroads of Development and Tumor Metastasis
Yang, J., & Weinberg, R. A. (2008) · Developmental Cell · doi:10.1016/j.devcel.2008.05.009 · Cited by 3,079
Epithelial-mesenchymal transition and its implications for fibrosis
Kalluri, R., & Neilson, E. G. (2003) · Journal of Clinical Investigation · doi:10.1172/jci20530 · Cited by 2,715
Self-citationTumour invasion and metastasis initiated by microRNA-10b in breast cancer
Ma, L., Teruya-Feldstein, J., & Weinberg, R. A. (2007) · Nature · doi:10.1038/nature06174 · Cited by 2,605
Research works printed but not linked: 8
- Kalluri, 2003, J. Clin. Invest., 112, 1776, 10.1172/JCI200320530 · DOI
- Xue, 2003, Cancer Res., 63, 3386
- Colwell, 2005, Adv. Biochem. Eng. Biotechnol., 93, 83
- Sommers, 1989, Cancer Res., 49, 4258
- Wernert, 2001, Anticancer Res., 21, 2259
- Higgins, 2007, J. Clin. Invest., 117, 3810
- Bates, 2005, J. Clin. Invest., 115, 339, 10.1172/JCI200523183 · DOI
- Gabbiani, 1981, Am. J. Pathol., 104, 206
Cited by
Sorted by citations
Items 301–400 of 1,004
Shukla, V. C., Higuita‐Castro, N., Nana-Sinkam, P. S., & Ghadiali, S. N. (2016) · Journal of Biomedical Materials Research Part A · doi:10.1002/jbm.a.35655 · Cited by 95
“In addition to morphological changes, EMT is commonly characterized by changes in biochemical signaling.(12) One of the most prominent biochemical changes during EMT is “cadherin switching,” where cells lose epithelial”
BackgroundIn Vitro Expansion of Corneal Endothelial Cells on Biomimetic Substrates
Palchesko, R. N., Lathrop, K. L., Funderburgh, J. L., & Feinberg, A. W. (2015) · Scientific Reports · doi:10.1038/srep07955 · Cited by 90
Chen, Y. S., Mathias, R. A., Mathivanan, S., Kapp, E. A., Moritz, R. L., Zhu, H., & Simpson, R. J. (2010) · Molecular & Cellular Proteomics · doi:10.1074/mcp.m110.001131 · Cited by 88
Epithelial-Mesenchymal Interactions in Biliary Diseases
Fabris, L., & Strazzabosco, M. (2011) · Seminars in Liver Disease · doi:10.1055/s-0031-1272832 · Cited by 90
LncRNA ANCR down-regulation promotes TGF-β-induced EMT and metastasis in breast cancer
Li, Z., Dong, M., Fan, D., Hou, P., Li, H., Liu, L., Lin, C., Liu, J., Su, L., Wu, L., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.18622 · Cited by 91
Prognostic significance of E-cadherin and N-cadherin expression in Gliomas
Noh, M., Oh, S.-J., Ahn, E., Kim, Y. J., Jung, T., Jung, S., Kim, K. K., Lee, J.-H., Lee, K., & Moon, K. (2017) · BMC Cancer · doi:10.1186/s12885-017-3591-z · Cited by 89
“Epithelial cell plasticity is rigorously redirected to display increased mesenchymal cadherins including N-cadherin or cadherin-11 and to convert immotile parent epithelial cells to motile cells with enhanced invasive properties [23, 24].”
BackgroundDing, L., Zhang, Z., Shang, D., Cheng, J., Yuan, H., Wu, Y., Song, X., & Jiang, H. (2013) · Journal of Oral Pathology and Medicine · doi:10.1111/jop.12143 · Cited by 89
Liu, Y., Zhang, J.-B., Qin, Y., Wang, W., Wei, L., Teng, Y., Guo, L., Zhang, B., Lin, Z., Liu, J., et al. (2013) · Hepatology · doi:10.1002/hep.26398 · Cited by 105
“, vimentin).(2) EMT has a crucial role in the progression and metastasis of multiple cancers including HCC.”
BackgroundLiu, Z., Chen, L., Zhang, X., Xu, X., Xing, H., Zhang, Y., Li, W., Yu, H., Zeng, J., & Jia, J. (2014) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.12209 · Cited by 89
Regulation of FN1 degradation by the p62/SQSTM1-dependent autophagy–lysosome pathway in HNSCC
Liu, X., Meng, L., Li, X., Li, D., Liu, Q., Chen, Y., Li, X., Bu, W., & Sun, H. (2020) · International Journal of Oral Science · doi:10.1038/s41368-020-00101-5 · Cited by 90
Javadrashid, D., Baghbanzadeh, A., Derakhshani, A., Leone, P., Silvestris, N., Racanelli, V., Solimando, A. G., & Baradaran, B. (2021) · Biomedicines · doi:10.3390/biomedicines9040373 · Cited by 90
“In carcinoma cells, type 3 EMT exists and is considered necessary for invasion, intravasation, extravasation, spread, and metastasis during the tumor growth process [40].”
Backgroundp16INK4A Represses the paracrine tumor-promoting effects of breast stromal fibroblasts
Al‐Ansari, M. M., Hendrayani, S., Shehata, A. I., & Aboussekhra, A. (2012) · Oncogene · doi:10.1038/onc.2012.270 · Cited by 88
Na,K-ATPase Subunits as Markers for Epithelial-Mesenchymal Transition in Cancer and Fibrosis
Langhans, S. A., Huynh, T. P., Wolle, D. G., Espineda, C. E., Inge, L. J., Skay, A., Lassman, C., Nicholas, S. B., Harper, J. F., Reeves, A. E., et al. (2010) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-09-0832 · Cited by 89
“This process involves the loss of cell-cell adhesion and intercellular junctions, destruction of the basement membrane, reorganization of the actin cytoskeleton, enhanced migratory capacity and invasiveness, activation of transcription factors, and downregulation of epithelial markers and expression of mesenchymal gen…”
BackgroundCancer cells remodel themselves and vasculature to overcome the endothelial barrier
Shenoy, A. K., & Lu, J. (2014) · Cancer Letters · doi:10.1016/j.canlet.2014.10.031 · Cited by 89
“of mesenchymal genes like N-cadherin, vimentin, fibronectin, and smooth muscle α actin (α-SMA) [17,18].”
BackgroundPothoven, K. L., & Schleimer, R. P. (2017) · Tissue Barriers · doi:10.1080/21688370.2017.1341367 · Cited by 89
SERPINB3 induces epithelial–mesenchymal transition
Quarta, S., Vidalino, L., Turato, C., Ruvoletto, M., Calabrese, F., Valente, M., Cannito, S., Fassina, G., Parola, M., Gatta, A., et al. (2010) · The Journal of Pathology · doi:10.1002/path.2708 · Cited by 87
“That EMT is associated with meatastasis is based on the observation that acquisition of mesenchymal markers such as vimentin, nuclear expression of β-catenin and loss of epithelial adhesion molecules, such as E-cadherin, were associated with increased metastatic potential [32].”
BackgroundA comparison of epithelial-to-mesenchymal transition and re-epithelialization
Leopold, P. L., Vincent, J., & Wang, H. (2012) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2012.07.003 · Cited by 93
“More recently, three distinct manifestations of EMT have been proposed [4,5] based on stages of development and associated biomarkers such that the EMT commonly associated with cancer metastasis (Type III) can be clearly differentiated from the involvement of EMT in either”
Clinical implication of ZEB-1 and E-cadherin expression in hepatocellular carcinoma (HCC)
Hashiguchi, M., Ueno, S., Sakoda, M., Iino, S., Hiwatashi, K., Minami, K., Ando, K., Mataki, Y., Maemura, K., Shinchi, H., et al. (2013) · BMC Cancer · doi:10.1186/1471-2407-13-572 · Cited by 86
“A variety of transcription factors including the zinc finger Snail homologues (Snail1, Snail2/Slug, and Snail3) and several basic helix-loop-helix factors such as Twist, ZEB1, and ZEB2, all interact with the E-box element within the proximal region of the E-cadherin promoter [5,8,10,11].”
Li, J., Liu, J., Yang, J., Li, P., Mao, X., Li, W., & Liu, P. (2014) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-014-0070-0 · Cited by 90
“E-cadherin is an important cancer metastasis suppressor and is required for cell-cell adhesion in the epithelial tissue [22].”
BackgroundShen, X.-Y., Zheng, L., Huang, J., Kong, H., Chang, Y.-J., Wang, F., & Xin, H. (2019) · RNA Biology · doi:10.1080/15476286.2019.1644591 · Cited by 86
“EMTs are characterized with a lower level of key epithelial marker (E-cadherin), and a higher expression of mesenchymal marker (β-catenin and vimentin) which are needed for cell migration and invasion [9,10].”
BackgroundAndrogen Depletion Induces Senescence in Prostate Cancer Cells through Down-regulation of Skp2
Pernicová, Z., Slabáková, E., Kharaishvili, G., Bouchal, J., Král, M., Kunická, Z., Machala, M., Kozubı́k, A., & Souček, K. (2011) · Neoplasia · doi:10.1593/neo.11182 · Cited by 87
Fabris, L., Cadamuro, M., Moserle, L., Dziura, J. D., Cong, X., Sambado, L., Nardo, G., Sonzogni, A., Colledan, M., Furlanetto, A., et al. (2011) · Hepatology · doi:10.1002/hep.24466 · Cited by 86
“During this process, some molecular programs typical of the mesenchymal phenotype are activated, as shown by the expression of specific cell surface proteins, cytoskeletal proteins, extracellular matrix-degrading enzymes, and transcription factors.(4) One such proteins is S100A4, a member of the S100 family of small c…”
Liu, S., Liu, L., Ye, W., Ye, D., Wang, T., Guo, W., Liao, Y., Xu, D., Song, H., Zhang, L., et al. (2016) · Scientific Reports · doi:10.1038/srep38834 · Cited by 86
Epithelial to mesenchymal transition as a biomarker in renal fibrosis: are we ready for the bedside?
Galichon, P., & Hertig, A. (2011) · Fibrogenesis & Tissue Repair · doi:10.1186/1755-1536-4-11 · Cited by 88
“It is important to use multiple markers simultaneously to detect the coordinated changes associated with EMT in the epithelial structures [31].”
Asaduzzaman, M., Constantinou, S., Min, H., Gallon, J., Lin, M.-L., Singh, P., Raguz, S., Ali, S., Shousha, S., Coombes, R. C., et al. (2017) · Breast Cancer Research and Treatment · doi:10.1007/s10549-017-4202-z · Cited by 86
“This phenotype involves major cellular reprogramming highlighted in the EP300 signature described here with downregulation of cell adhesion molecules, such as EPCAM5 and EPCAM6, and upregulation of collagens (COL12A1 and COL4A5) and mesenchymal OB-cadherin (CDH11), a characteristic EMT marker [39].”
BackgroundYang, Z., García, A., Xu, S., Powell, D. R., Vertino, P. M., Singh, S. V., & Marcus, A. I. (2013) · PLoS ONE · doi:10.1371/journal.pone.0075069 · Cited by 85
“aggressive cell lines and tumors [46-53], and correlates with”
BackgroundAi, J., Tang, Q., Wu, Y., Xu, Y., Feng, T., Zhou, R., Chen, Y., Gao, X., Zhu, Q., Yue, X., et al. (2011) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/djr360 · Cited by 84
Bai, X., Geng, J., Zhou, Z., Tian, J., & Xiao, L. (2016) · Scientific Reports · doi:10.1038/srep20475 · Cited by 85
Charbonney, E., Speight, P., Masszi, A., Nakano, H., & Kapus, A. (2011) · Molecular Biology of the Cell · doi:10.1091/mbc.e11-04-0335 · Cited by 84
“During fibrogenic (type 2) EMT, epithelial cells lose their strong intercellular contacts and apicobasal polarity and acquire fibroblast-like features, such as elongated shape, increased extracellular matrix (ECM) production, and motility (Zeisberg and Neilson, 2009).”
BackgroundMicrofluidic co-culture system for cancer migratory analysis and anti-metastatic drugs screening
Mi, S., Du, Z., Xu, Y., Wu, Z., Qian, X., Zhang, M., & Sun, W. (2016) · Scientific Reports · doi:10.1038/srep35544 · Cited by 85
“This is an important feature of EMT 46,47 , and we also observed a morphological change in the HMEpiC cells co-cultured with cancer cells (Fig.”
Epithelial-to-Mesenchymal Transition in Fibrosis: Concepts and Targeting Strategies
Lovisa, S. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.737570 · Cited by 84
Kaimori, A., Potter, J. J., Choti, M. A., Ding, Z., Mezey, E., & Koteish, A. A. (2010) · Hepatology · doi:10.1002/hep.23765 · Cited by 84
“Type 1 EMT and type 3 EMT occur in the absence of inflammation, whereas type 2 EMT, the focus of this article, occurs in the presence of inflammation.(9-12) EMT is not an all or nothing phenomenon, and it encompasses a spectrum of such changes: we have previously referred to this phenomenon as an EMT state in referenc…”
BackgroundMethodA new strategy to measure intercellular adhesion forces in mature cell-cell contacts
Sancho, A., Vandersmissen, I., Craps, S., Luttun, A., & Gröll, J. (2017) · Scientific Reports · doi:10.1038/srep46152 · Cited by 86
“Lastly, we investigated if MSX1 overexpression resulted in cytoskeletal rearrangements known to occur during EndMT 35 .”
Sohal, S. S., Mahmood, M. Q., & Walters, E. H. (2014) · Clinical and Translational Medicine · doi:10.1186/s40169-014-0033-2 · Cited by 83
“When associated with angiogenesis (Type-III EMT) it may well also be a link with the development of lung (airway) cancer which is closely associated with COPD.”
BackgroundResultInfluentialGulei, D., Magdo, L., Jurj, A. M., Ráduly, L., Cojocneanu, R., Moldovan, A. I., Moldovan, C. S., Florea, A., Paşca, S., Pop, L., et al. (2018) · Cell Death and Disease · doi:10.1038/s41419-017-0102-8 · Cited by 83
Wang, M., Yan, J., Cao, X., Hua, P., & Li, Z. (2019) · Biochemical Pharmacology · doi:10.1016/j.bcp.2019.113775 · Cited by 83
Chen, X.-H., Liu, Z., Zhang, G., Wei, W., Wang, X., Wang, H., Ke, H., Zhang, F., Wang, H.-S., Cai, S., et al. (2015) · Molecular Immunology · doi:10.1016/j.molimm.2014.12.017 · Cited by 86
the Epithelial-to-Mesenchymal Transition in Liver Fibrosis: Here Today, Gone Tomorrow?
Wells, R. G. (2010) · Hepatology · doi:10.1002/hep.23529 · Cited by 83
“One recently proposed scheme divides EMT into three distinct categories: type 1 occurring in development, type 2 in fibrosis, and type 3 in cancer and metastasis.(6,8) Type 1 EMT yields mesenchymal cells whereas type 2 yields fibroblasts which produce collagen, although they may or may not later become myofibroblasts.”
BackgroundJiang, B., Zhang, T., Liu, F., Sun, Z., Shi, H., Hua, D., & Yang, C. G. (2016) · Oncotarget · doi:10.18632/oncotarget.9035 · Cited by 82
Plasticity of Cancer Cell Invasion—Mechanisms and Implications for Therapy
Boekhorst, V. T., & Friedl, P. (2016) · Advances in cancer research · doi:10.1016/bs.acr.2016.07.005 · Cited by 89
Wen, Y., Lee, W.-J., Tan, P., Yang, S., Hsiao, M., Lee, L.-M., & Chien, M. (2015) · Oncotarget · doi:10.18632/oncotarget.4229 · Cited by 81
Yu, G., Herazo‐Maya, J. D., Nukui, T., Romkes, M., Parwani, A. V., Juan-Guardela, B. M., Robertson, J. V., Gauldie, J., Siegfried, J. M., Kaminski, N., et al. (2014) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201310-1903oc · Cited by 85
Xiao, J., Gong, Y., Chen, Y., Yu, D., Wang, X., Zhang, X., Dou, Y., Liu, D., Cheng, G., Lu, S., et al. (2017) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00428.2016 · Cited by 83
Role of chemokine receptor CXCR7 in bladder cancer progression
Hao, M., Zheng, J., 侯恺林, Wang, J., Chen, X., Lu, X., 卜, 军., Xu, C., Shen, K., & Wang, J. (2012) · Biochemical Pharmacology · doi:10.1016/j.bcp.2012.04.007 · Cited by 82
“To test the possibility, we assessed the expression of EMT marker proteins as previously reported [27].”
ResultAlimperti, S., You, H., George, T., Agarwal, S. K., & Andreadis, S. T. (2014) · Journal of Cell Science · doi:10.1242/jcs.134833 · Cited by 82
“During the process of EMT, the expression of E-cadherin is repressed, whereas cadherin-11 and cadherin-2 are upregulated, indicating a possible role of cadherins in diverse biological processes such as fibrosis or carcinogenesis (Tomita et al., 2000).”
BackgroundWang, D., Huang, J., & Hu, Z. (2011) · Molecular & Cellular Proteomics · doi:10.1074/mcp.m111.011932 · Cited by 85
“the cytoskeletal reorganization after DDX5 knockdown was not due to MET (28).”
BackgroundRyu, M., Migliorini, A., Miosge, N., Groß, O., Shankland, S. J., Brinkkoetter, P. T., Hagmann, H., Romagnani, P., Liapis, H., & Anders, H. (2012) · The Journal of Pathology · doi:10.1002/path.4046 · Cited by 82
“This phenomenon, named epithelial–mesenchymal transition (EMT) by some authors [40–42], is proposed to occur in tubular epithelial cells, triggered by TGF-β [55,61].”
BackgroundAR Variant ARv567es Induces Carcinogenesis in a Novel Transgenic Mouse Model of Prostate Cancer
Liu, G., Sprenger, C. C. T., Sun, S., Epilepsia, K. S., Haugk, K. L., Zhang, X., Coleman, I. M., Nelson, P. S., & Plymate, S. R. (2013) · Neoplasia · doi:10.1593/neo.13784 · Cited by 83
Sohal, S. S., Soltani, A., Reid, D. W., Ward, C., Wills, K. E., Muller, H. K., & Walters, E. H. (2014) · International Journal of COPD · doi:10.2147/copd.s63911 · Cited by 82
“3,4 These findings were based on immunostaining for acknowledged “classic” empiric EMT markers 10,11,25,26 and based especially on criteria for in vivo research on EMT as suggested by Zeisberg and Neilson.”
InfluentialYin, G., Alvero, A. B., Craveiro, V., Holmberg, J. C., Fu, H., Montagna, M. K., Yang, Y., Chefetz, I., Nuti, S. L., Rossi, M. R., et al. (2012) · Oncogene · doi:10.1038/onc.2012.33 · Cited by 81
“Western blot analysis further confirmed the induction of mesenchymal markers VIMENTIN, FOXC2, SLUG, and TWIST1 (Fig.”
InfluentialSaito, S., OKABE, H., Watanabe, M., Ishimoto, T., Iwatsuki, M., Baba, Y., Tanaka, Y., Kurashige, J., Miyamoto, Y., & Baba, H. (2013) · Oncology Reports · doi:10.3892/or.2013.2273 · Cited by 81
“This process involves the acquisition of the expression of mesenchymal molecules, such as vimentin and fibronectin, together with the loss of epithelial cell adhesion molecules such as E-cadherin (7).”
BackgroundHe (2010) · Oncology Reports · doi:10.3892/or_00000794 · Cited by 81
Voutsadakis, I. A. (2012) · Journal of Biomedical Science · doi:10.1186/1423-0127-19-67 · Cited by 86
“In vitro and in vivo criteria for the confirmation of EMT have been established and fall into two broad categories [4].”
BackgroundRanieri, D., Rosato, B., Nanni, M., Magenta, A., Belleudi, F., & Torrisi, M. R. (2015) · Oncotarget · doi:10.18632/oncotarget.6706 · Cited by 83
“Based on the different features and biomarkers involved, EMT has been classified into three distinct processes [19,20]: the EMT type III (commonly associated with cancer progression and simply named EMT) is characterized by the migration of isolated mesenchymal-like cells and is clearly distinct from the EMT involved…”
BackgroundZhao, H., Bian, H., Bu, X., Zhang, S., Zhang, P., Yu, J., Lai, X., Li, D., Zhu, C., Yao, L., et al. (2016) · Molecular Therapy · doi:10.1038/mt.2016.109 · Cited by 84
Lee, S.-J. (2014) · World Journal of Hepatology · doi:10.4254/wjh.v6.i4.207 · Cited by 82
Szatmári, T., & Dobra, K. (2013) · Frontiers in Oncology · doi:10.3389/fonc.2013.00310 · Cited by 90
“This ability to switch from epithelial to mesenchymal phenotype involves a simultaneous downregulation of epithelial markers including syndecan-1 and E-cadherin (46, 86, 87).”
BackgroundZhang, Y., Yan, W., & Chen, X. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.214585 · Cited by 84
Yang, X., Sarvestani, S. K., Moeinzadeh, S., He, X., & Jabbari, E. (2012) · Tissue Engineering Part A · doi:10.1089/ten.tea.2012.0333 · Cited by 86
“81,82 It is possible that the hydrogel stiffness shifts the balance of EMT by regulating the conformation of cell membrane receptors and cell polarity.”
Tang, O., Chen, X., Shen, S., Hahn, M., & Pollock, C. A. (2013) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00302.2012 · Cited by 81
“EMT has recently been categorized into three subtypes (3, 36): type 1 in embryogenesis, type 2 in epithelial or endothelial cells transitioning to resident tissue fibroblasts, and type 3 in epithelial carcinoma cells transitioning to metastatic tumor cells.”
Human trophoblast epithelial-mesenchymal transition in abnormally invasive placenta†
DaSilva‐Arnold, S. C., Zamudio, S., Al‐Khan, A., Alvarez‐Perez, J. R., Mannion, C. M., Koenig, C., Luke, D., Perez, A. M., Petroff, M. G., Alvarez, M., et al. (2018) · Biology of Reproduction · doi:10.1093/biolre/ioy042 · Cited by 80
“They suggested that this was the consequence of a shift, in AIP, to a mesenchymal phenotype, characteristic of the epithelial-mesenchymal transition (EMT) observed in embryonic development, wound healing and in cancer metastasis [11, 12].”
BackgroundQin, G., Xu, F., Qin, T., Zheng, Q., Shi, D., Xia, W., Tian, Y., Tang, Y., Wang, J., Xiao, X., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.5993 · Cited by 81
Xiao, W., Chen, X., Liu, X., Luo, L., Ye, S., & Liu, Y. (2014) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.12212 · Cited by 79
“In fact, it has been shown that all known EMT events during development, cancer and fibrosis appear to be associated with Snail activation [18, 29].”
BackgroundHepatitis C Virus Induces Epithelial-Mesenchymal Transition in Primary Human Hepatocytes
Bose, S. K., Meyer, K., Bisceglie, A. M. D., Ray, R. B., & RAY, R. K. (2012) · Journal of Virology · doi:10.1128/jvi.02016-12 · Cited by 81
“Type 1 EMT produces mesenchymal cells during embryogenesis, while type 2 EMT in adult or maturing tissues results in a fibroblast-like state (47).”
BackgroundInferring microRNA–mRNA causal regulatory relationships from expression data
Le, T. D., Liu, L., Tsykin, A., Goodall, G. J., Liu, B., Sun, B., & Li, J. (2013) · Bioinformatics · doi:10.1093/bioinformatics/btt048 · Cited by 81
“Especially, there are several genes in the sub-categories of cellular movement, invasion and migration, which have been identified as the functional bio-markers of EMT [35].”
BackgroundInfluentialSnodgrass, S. M., Cihil, K. M., Cornuet, P. K., Myerburg, M. M., & Swiatecka‐Urban, A. (2013) · PLoS ONE · doi:10.1371/journal.pone.0063167 · Cited by 79
“abundance of E- and N-cadherin, markers of the epithelial and mesenchymal cell phenotype, respectively [44].”
BackgroundYuan, Y., Li, D., Li, H., Wang, L., TIAN, G., & DONG, Y. (2015) · Molecular Medicine Reports · doi:10.3892/mmr.2015.4550 · Cited by 79
LARP7 suppresses P-TEFb activity to inhibit breast cancer progression and metastasis
Ji, X., Lu, H., Zhou, Q., & Luo, K. (2014) · eLife · doi:10.7554/elife.02907 · Cited by 79
Cui, H. S., Hong, A. R., Kim, J., Yu, J. H., Cho, Y. A., Joo, S. Y., & Seo, C. H. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19010124 · Cited by 80
“In particular, expression levels of N- and E-cadherin are closely involved in EMT [36], where the loss of E-cadherin is correlated with an upregulation of N-cadherin [37].”
BackgroundLi, X., Kong, X., Huo, Q., Guo, H., Yan, S., Yuan, C., Moran, M. S., Shao, C., & Yang, Q. (2011) · Cancer Science · doi:10.1111/j.1349-7006.2011.01919.x · Cited by 78
Sp1-mediated microRNA-182 expression regulates lung cancer progression
Yang, W., Chen, P.-H., Hsu, T., Fu, T.-F., Su, W., Liaw, H., Chang, W., & Hung, J. (2014) · Oncotarget · doi:10.18632/oncotarget.1608 · Cited by 78
The role of MTDH/AEG-1 in the progression of cancer.
Shi, X., & Wang, X. (2015) · PubMed Central · Cited by 79
Yang, M. H., Lee, J. H., Ko, J., Jung, S. H., Sethi, G., & Ahn, K. S. (2019) · Molecules · doi:10.3390/molecules24081584 · Cited by 78
Wei, R., Cortez Penso, N. E., Hackman, R. M., Wang, Y., & Mackenzie, G. G. (2019) · Nutrients · doi:10.3390/nu11081856 · Cited by 78
“Interestingly, in a mesenchymal state, an increased expression of Vimentin, ZEB1, and Snail, and a decreased expression of E-cadherin is often observed [33].”
BackgroundLi, S., Xie, Y., Zhang, W., Gao, J., Wang, M., Zheng, G., Yin, X., Xia, H., & Tao, X. (2014) · Journal of Surgical Research · doi:10.1016/j.jss.2014.06.055 · Cited by 78
Tang, M., Jiang, L., Lin, Y., Wu, X., Wang, K., He, Q., Wang, X., & Li, W. (2017) · Oncotarget · doi:10.18632/oncotarget.22136 · Cited by 78
Chen, X., Xiao, W., Chen, W., Luo, L., Ye, S., & Liu, Y. (2013) · Cell Death and Disease · doi:10.1038/cddis.2013.416 · Cited by 77
“In fact, most known EMT events during cancer development and fibrosis appear to be associated with Snail and Slug activation.(26) Therefore, we next investigated whether the effects of TSA on LECs EMT”
BackgroundCosta, L. C. M. C., LEITE, C. F., Cardoso, S. V., Loyola, A. M., de Faria, P. R., Souza, P. E. A., & Horta, M. C. R. (2015) · Journal of Applied Oral Science · doi:10.1590/1678-775720140187 · Cited by 77
Хромова, Н. В., Kopnin, P., Александровна, Р. В., & Kopnin, B. P. (2011) · Oncogene · doi:10.1038/onc.2011.330 · Cited by 79
“In fact, inhibition of VEGF-C production caused a suppression of vimentin and N-cadherin expression and induction of cytokeratins and E-cadherin expression, that is, changed the expression of a set of markers that are commonly used for detection of EMT (reviewed in Zeisberg and Neilson, 2009).”
BackgroundEpithelial-mesenchymal transition in morphogenesis, cancer progression and angiogenesis
Ribatti, D. (2017) · Experimental Cell Research · doi:10.1016/j.yexcr.2017.02.041 · Cited by 78
Ma, J., Zeng, S., Zhang, Y., Deng, G., Qu, Y., Guo, C., Yin, L., Han, Y., Cai, C., Li, Y., et al. (2017) · Cancer Letters · doi:10.1016/j.canlet.2017.09.041 · Cited by 77
Recent updates on the role of microRNAs in prostate cancer
Hassan, O., Ahmad, A., Sethi, S. N., & Sarkar, F. H. (2012) · Journal of Hematology & Oncology · doi:10.1186/1756-8722-5-9 · Cited by 77
“It is well known that NF- B plays an essential role in facilitating the processes of EMT induced by different factors through up-regulation of ZEB1 and ZEB2, which in turn suppress the expression of miR-200 family members by binding to the E-box sequence of the miR-200 promoter [69].”
BackgroundInfluentialPan, L., Liang, W., Gu, J., Zang, X., Huang, Z., Shi, H., Chen, J., Fu, M., Zhang, P., Xiao, X., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.23019 · Cited by 76
Khatib, A., Solaimuthu, B., Yosef, M. B., Rmaileh, A. A., Tanna, M., Oren, G., Frisch, M. S., Axelrod, J. H., Lichtenstein, M., & Shaul, Y. D. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2010275117 · Cited by 80
“HIF1α plays a regulatory role in the EMT program (60) as it represses E-cadherin expression (61) or activates the expression of the key EMT transcription factors such as TWIST (62), ZEB1, and ZEB2 (3).”
BackgroundInfluentialEpithelial‐mesenchymal transition as a fundamental mechanism underlying the cancer phenotype
Cervantes-Arias, A., Pang, L. Y., & Argyle, D. J. (2012) · Veterinary and Comparative Oncology · doi:10.1111/j.1476-5829.2011.00313.x · Cited by 77
Pathologic and molecular features of uterine carcinosarcomas
López‐García, M. Á., & Palacios, J. (2010) · Seminars in Diagnostic Pathology · doi:10.1053/j.semdp.2010.09.005 · Cited by 76
Epithelial-to-Mesenchymal Stem Cell Transition in a Human Organ: Lessons from Lichen Planopilaris
Imanishi, H., Ansell, D. M., Chéret, J., Harries, M. J., Bertolini, M., Sepp, N. T., Bı́ró, T., Poblet, E., Jiménez, F., Hardman, J. A., et al. (2017) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2017.09.047 · Cited by 76
Cai, Z., Cao, Y., Luo, Y., Hu, H., & Ling, H. Y. (2018) · Clinica Chimica Acta · doi:10.1016/j.cca.2018.04.033 · Cited by 77
SCFFBW7-mediated degradation of Brg1 suppresses gastric cancer metastasis
Huang, L.-Y., Zhao, J., Chen, H., Wan, L., Inuzuka, H., Guo, J., Fu, X., Zhai, Y., Lu, Z., Wang, X., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-06038-y · Cited by 78
Notch-dependent EMT is attenuated in patients with aortic aneurysm and bicuspid aortic valve
Kostina, A. S., Uspensky, V., Irtyuga, O. B., Ignatieva, E. V., Freylikhman, O., Gavriliuk, N., Моисеева, О. М., Zhuk, S., Tomilin, A. N., Kostareva, A. A., et al. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.02.006 · Cited by 73
“We made additional screening of 11 genes previously described as markers of EMT [29]: PECAM1, VWF, ACTA2, COL1A1, FOXC2, CDH2 (N-cadherin), TAGLN (SM22α), TWIST1,”
BackgroundSingle-cell RNA sequencing uncovers a neuron-like macrophage subset associated with cancer pain
Tang, P. C., Chung, J. Y., Liao, J., Chan, M. K., Chan, A. S. W., Cheng, G., Li, C., Huang, X., Ng, C. S. H., Lam, E. W. ‐., et al. (2022) · Science Advances · doi:10.1126/sciadv.abn5535 · Cited by 77
“This system allows us to trace origins of the macrophage lineage cells, even when their lineage markers were lost during maturation and differentiation ( 30 ).”
Lu, L., Luo, F., Liu, Y., Liu, X., Shi, L., Lü, X., & Liu, Q. (2015) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2015.09.016 · Cited by 75
Identification of cancer stem cells in vincristine preconditioned SGC7901 gastric cancer cell line
Xue, Z., Yan, H. M., Li, J., Liang, S., Cai, X., Chen, X., Wu, Q., Gao, L., Wu, K., Nie, Y., et al. (2011) · Journal of Cellular Biochemistry · doi:10.1002/jcb.23356 · Cited by 75
Epithelial and endothelial cell plasticity in chronic obstructive pulmonary disease (COPD)
Sohal, S. S. (2017) · Respiratory Investigation · doi:10.1016/j.resinv.2016.11.006 · Cited by 75
Effects of microRNA‐30a on migration, invasion and prognosis of hepatocellular carcinoma
Liu, Z., Tu, K., & Liu, Q. (2014) · FEBS Letters · doi:10.1016/j.febslet.2014.06.037 · Cited by 74
“Reduced E-cadherin protein expression and increased expression of vimentin protein are used as markers indicating an epithelial cell has undergone EMT [13].”
BackgroundNovel clinical therapeutics targeting the epithelial to mesenchymal transition
Kothari, A. N., Mi, Z., Zapf, M. A. C., & Kuo, P. C. (2014) · Clinical and Translational Medicine · doi:10.1186/s40169-014-0035-0 · Cited by 74
“revert renal fibrosis in mice [28].”
Bunel, V., Antoine, M., Nortier, J., Duez, P., & Stévigny, C. (2015) · Toxicology in Vitro · doi:10.1016/j.tiv.2014.12.017 · Cited by 74
Dazert, E., Colombi, M., Boldanova, T., Moes, S., Adametz, D., Quagliata, L., Röth, V., Terracciano, L., Heim, M. H., Jenoe, P., et al. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1523434113 · Cited by 73
“Collectively, these changes suggest that EMT occurred in the tumor, during tumor progression and/or in response to sorafenib (45, 46).”
BackgroundBufalo, F. D., Manzo, T., Hoyos, V., Yagyu, S., Caruana, I., Jacot, J. G., Benavides, O. M., Rosen, D. G., & Brenner, M. K. (2016) · Biomaterials · doi:10.1016/j.biomaterials.2016.01.030 · Cited by 73
Cadherin-11 is a novel regulator of extracellular matrix synthesis and tissue mechanics
Row, S., Liu, Y., Alimperti, S., Agarwal, S. K., & Andreadis, S. T. (2016) · Journal of Cell Science · doi:10.1242/jcs.183772 · Cited by 74
“CDH11 is expressed in osteoblasts and mesenchymal cells as well as in epithelial cells undergoing epithelial–mesenchymal transition (EMT), as for example during progression of cancer cells into a metastatic state (Kimura et al., 1995; Tomita et al., 2000; Zeisberg and Neilson, 2009).”
Background
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review