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Guidelines and definitions for research on epithelial-mesenchymal transition.

ABSTRACT: Epithelial-mesenchymal transition (EMT) encompasses dynamic changes in cellular organization from epithelial to mesenchymal phenotypes, which leads to functional changes in cell migration and invasion. EMT occurs in a diverse range of physiological and pathological conditions and is driven by a conserved set of inducing signals, transcriptional regulators and downstream effectors. With over 5,700 publications indexed by Web of Science in 2019 alone, research on EMT is expanding rapidly. This growing interest warrants the need for a consensus among researchers when referring to and undertaking research on EMT. This Consensus Statement, mediated by 'the EMT International Association' (TEMTIA), is the outcome of a 2-year-long discussion among EMT researchers and aims to both clarify the nomenclature and provide definitions and guidelines for EMT research in future publications. We trust that these guidelines will help to reduce misunderstanding and misinterpretation of research data generated in various experimental models and to promote cross-disciplinary collaboration to identify and address key open questions in this research field. While recognizing the importance of maintaining diversity in experimental approaches and conceptual frameworks, we emphasize that lasting contributions of EMT research to increasing our understanding of developmental processes and combatting cancer and other diseases depend on the adoption of a unified terminology to describe EMT.

SUBMITTER: Yang J

PROVIDER: S-EPMC7250738 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Guidelines and definitions for research on epithelial-mesenchymal transition.

Yang Jing J Antin Parker P Berx Geert G Blanpain Cédric C Brabletz Thomas T Bronner Marianne M Campbell Kyra K Cano Amparo A Casanova Jordi J Christofori Gerhard G Dedhar Shoukat S Derynck Rik R Ford Heide L HL Fuxe Jonas J García de Herreros Antonio A Goodall Gregory J GJ Hadjantonakis Anna-Katerina AK Huang Ruby Y J RYJ Kalcheim Chaya C Kalluri Raghu R Kang Yibin Y Khew-Goodall Yeesim Y Levine Herbert H Liu Jinsong J Longmore Gregory D GD Mani Sendurai A SA Massagué Joan J Mayor Roberto R McClay David D Mostov Keith E KE Newgreen Donald F DF Nieto M Angela MA Puisieux Alain A Runyan Raymond R Savagner Pierre P Stanger Ben B Stemmler Marc P MP Takahashi Yoshiko Y Takeichi Masatoshi M Theveneau Eric E Thiery Jean Paul JP Thompson Erik W EW Weinberg Robert A RA Williams Elizabeth D ED Xing Jianhua J Zhou Binhua P BP Sheng Guojun G

Nature reviews. Molecular cell biology 20200416 6

Epithelial-mesenchymal transition (EMT) encompasses dynamic changes in cellular organization from epithelial to mesenchymal phenotypes, which leads to functional changes in cell migration and invasion. EMT occurs in a diverse range of physiological and pathological conditions and is driven by a conserved set of inducing signals, transcriptional regulators and downstream effectors. With over 5,700 publications indexed by Web of Science in 2019 alone, research on EMT is expanding rapidly. This gro ...[more]

PMID: 32300252

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Project description:DCLK1 and Lgr5 have recently been identified as markers of quiescent and cycling stem cells in the small intestinal crypts, respectively. Epithelial-mesenchymal transition (EMT) is a key development program that is often activated during cancer invasion and metastasis, and also imparts a self-renewal capability to disseminating cancer cells. Utilizing the Citrobacter rodentium (CR)-induced transmissible murine colonic hyperplasia (TMCH) model, we observed a relative decrease in DCLK1 expression in the colonic crypts, with significant shift towards stromal staining at peak (12 days post infection) hyperplasia, whereas staining for Lgr5 and Msi-1 increased several fold. When hyperplasia was regressing (days 20-34), an expansion of DCLK1+ve cells in the CR-infected crypts compared with that seen in uninfected control was recorded. Purified colonic crypt cells exhibiting epigenetic modulation of the transforming growth factor-β (TGFβ), Wnt and Notch pathways on 12 or 34 days post infection formed monolayers in vitro, and underwent trans-differentiation into fibroblast-like cells that stained positive for vimentin, fibronectin and DCLK1. These cells when trypsinized and regrown in soft agar, formed colonospheres/organoids that developed into crypt-like structures (colonoids) in Matrigel and stained positive for DCLK1. Mice exhibiting 12 or 34 days of TMCH were given azoxymethane once for 8 h (Gp1) or weekly for 3 weeks (Gp2), and subjected to crypt isolation. Crypt cells from Gp1 animals formed monolayers as well as colonospheres in soft agar and nodules/tumors in nude mice. Crypt cells isolated from Gp2 animals failed to form the monolayers, but developed into colonospheres in soft agar and nodules/tumors in nude mice. Thus, both hyperplasia and increased presence of DCLK1+ve cells promote cellular transformation in response to a second hit. The TMCH model, therefore, provides an excellent template to study how alterations in intestinal stem cells promote trans-differentiation, crypt regeneration or colon carcinogenesis following bacterial infection.

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Guidelines and definitions for research on epithelial-mesenchymal transition.

Publications

Guidelines and definitions for research on epithelial-mesenchymal transition.

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