Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (521 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Phenotypic changes of epithelial cells to mesenchyme type, which increase cell mobility critical in many developmental processes such as neural tube development. neoplasm metastasis and disease progression may also induce this transition.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Epithelial Mesenchymal Transition; Transition, Epithelial-Mesenchymal; Epithelial-Mesenchymal Transformation; Epithelial Mesenchymal Transformation; Transformation, Epithelial-Mesenchymal.
Where it fits in the MeSH classification
- Broader topics
- Cell Transdifferentiation
- Narrower topics
- Endothelial-Mesenchymal Transition
Related concepts
- Epithelial Cells
- Mesoderm
- Neural Tube
- Neoplasm Metastasis
- Disease Progression
Research landscape
PubMed indexes 31,329 records tagged with the MeSH heading “Epithelial-Mesenchymal Transition” (counts retrieved 2026-10-29). 15,096 of them (48.2%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 16,579 records.
Reviews account for 3,950 records (12.6%) and meta-analyses for 38. Randomized controlled trials number 24 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 17 |
| 2010-2019 | 16,579 |
| 2020 onward | 15,096 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,950 | 12.6% |
| Meta-analyses | 38 | 0.1% |
| Randomized controlled trials | 24 | 0.1% |
Method: PubMed query "Epithelial-Mesenchymal Transition"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| RBMX2 links Mycobacterium bovis infection to epithelial-mesenchymal transition and lung cancer progression | 2025 | Research article Design not recorded in structured metadata | 12 | cc by PMID 41277807 · DOI · PMC12643470 |
| TGFβ induces an atypical EMT to evade immune mechanosurveillance in lung adenocarcinoma dormant metastasis | 2026 | Research article Design not recorded in structured metadata | 10 | cc by PMID 41492090 · DOI · PMC12858408 |
| TWIST1 drives endothelial-to-mesenchymal-transition to stabilize atherosclerotic plaques | 2026 | Research article Design not recorded in structured metadata | 9 | cc by PMID 41708636 · DOI · PMC13031644 |
RBMX2 links Mycobacterium bovis infection to epithelial-mesenchymal transition and lung cancer progression [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Tuberculosis (TB) is a complex disease caused by the interaction of pathogen, host, and environmental factors.
- Closing excerpt
- These findings provide new insight into TB pathogenesis and highlight RBMX2 as a potential target for TB vaccine and therapeutic development.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (214 words)
Tuberculosis (TB) is a complex disease caused by the interaction of pathogen, host, and environmental factors. In 2022, TB affected 10.6 million people and caused 1.3 million deaths globally. In high-burden zoonotic TB regions, Mycobacterium bovis accounts for ~10% of human TB cases. The immune evasion and latency of Mycobacterium tuberculosis hinder understanding of host responses. Here, we identify RNA-binding motif protein X-linked 2 (RBMX2) as a novel host factor facilitating M. bovis infection. RBMX2 expression is significantly upregulated in multiple cell types, including EBL, BoMac, bovine alveolar primary cells, and human A549 cells. Multi-omics analyses, cell adhesion assays, and ChIP-PCR demonstrate that RBMX2 suppresses cell adhesion and tight junctions while enhancing M. bovis adhesion and invasion via p65 signaling. Integrated transcriptomic, proteomic, and metabolomic data reveal that RBMX2 regulates epithelial-mesenchymal transition (EMT), a process linked to cancer progression. TIMER2.0 analysis shows elevated RBMX2 expression in lung adenocarcinoma and lung squamous cell carcinoma tissues, validated by immunofluorescence. Using an M. bovis-induced BoMac-EBL EMT model and H1299 cells, we show that RBMX2 promotes EMT through p65/MMP-9 pathway activation. Collectively, RBMX2 is a novel host factor that enhances M. bovis infection and drives infection-induced EMT. These findings provide new insight into TB pathogenesis and highlight RBMX2 as a potential target for TB vaccine and therapeutic development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41277807 · DOI · PMC12643470
TGFβ induces an atypical EMT to evade immune mechanosurveillance in lung adenocarcinoma dormant metastasis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Different forms of epithelial-to-mesenchymal transition (EMT) manifest during tumor progression.
- Closing excerpt
- Thus, quiescent LUAD metastatic progenitors undergo an atypical EMT to avert immune surveillance during TGFβ-driven metastatic dormancy.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Different forms of epithelial-to-mesenchymal transition (EMT) manifest during tumor progression. Little is known about the mechanistic basis and functional role of these distinct EMTs. We explored this question in lung adenocarcinoma (LUAD) primitive progenitors, which are competent to enter dormancy in response to transforming growth factor-β (TGFβ) upon metastatic dissemination. The TGFβ response in these cells includes growth arrest and a full EMT that subsequently transitions into an atypical mesenchymal state of round morphology and lacking actin stress fibers. TGFβ drives this transition by inducing expression of the actin depolymerizing protein gelsolin, which converts a migratory, stress-fiber-rich phenotype into a cortical actin-rich, spheroidal state. This transition lowers the biomechanical stiffness of metastatic progenitors and protects them from killing by cytotoxic lymphocytes. Gelsolin-deficient LUAD progenitors can enter dormancy but succumb to immune surveillance. Thus, quiescent LUAD metastatic progenitors undergo an atypical EMT to avert immune surveillance during TGFβ-driven metastatic dormancy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41492090 · DOI · PMC12858408
TWIST1 drives endothelial-to-mesenchymal-transition to stabilize atherosclerotic plaques [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Rupture of unstable atherosclerotic plaques is a major cause of mortality.
- Closing excerpt
- These findings challenge the prevailing view that endothelial-to-mesenchymal transition uniquely destabilizes plaques, by suggesting that TWIST1-driven endothelial-to-mesenchymal transition can promote plaque stability, offering new insights into atherosclerosis pathophysiology and therapeutic potential.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (158 words)
Rupture of unstable atherosclerotic plaques is a major cause of mortality. Endothelial-to-mesenchymal transition associates with advanced atherosclerotic plaques and contributes to plaque progression. We examined the role of Twist1, a transcription factor that drives endothelial-to-mesenchymal transition, in plaque progression by inducible deletion from endothelial cells in hypercholesterolemic mice (Twist1ECKO Apo-/-). Single-cell RNA sequencing coupled to endothelial cell-tracking reveals that Twist1 promotes endothelial-to-mesenchymal transition in advanced atherosclerotic plaques. Histological analyses demonstrate that endothelial Twist1 promotes plaque growth and hallmarks of plaque stability (collagen, ACTA2-positive cells) and reduces features of instability (necrosis, macrophage accumulation). Analysis of cultured human aortic endothelial cells shows that TWIST1 contributes to endothelial-to-mesenchymal transition by promoting migration and proliferation through the transcriptional coactivator PELP1. Additionally, TWIST1 promotes endothelial cell proliferation via AEBP1-dependent upregulation of COL4A1. These findings challenge the prevailing view that endothelial-to-mesenchymal transition uniquely destabilizes plaques, by suggesting that TWIST1-driven endothelial-to-mesenchymal transition can promote plaque stability, offering new insights into atherosclerosis pathophysiology and therapeutic potential.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41708636 · DOI · PMC13031644
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis [4]
- Research article EMT, MET, Plasticity, and Tumor Metastasis [5]
- Research article Circulating tumor cells: biology and clinical significance [6]
- Research article Dynamic EMT: a multi-tool for tumor progression [7]
- Research article The double-edged roles of ROS in cancer prevention and therapy [8]
- Research article Linking EMT programmes to normal and neoplastic epithelial stem cells [9]
References
- Wang C, Peng Y, Yang H, Jiang Y, Khalid AK, Zhang K, et al.. RBMX2 links Mycobacterium bovis infection to epithelial-mesenchymal transition and lung cancer progression. . 2025. PMID 41277807 · DOI · PMC12643470
- Wang Z, Elbanna Y, Godet I, Gan S, Peters L, Lampe G, et al.. TGFβ induces an atypical EMT to evade immune mechanosurveillance in lung adenocarcinoma dormant metastasis. . 2026. PMID 41492090 · DOI · PMC12858408
- Tardajos Ayllon B, Diagbouga M, Das A, Tian S, Edsfeldt A, Kalucka J, et al.. TWIST1 drives endothelial-to-mesenchymal-transition to stabilize atherosclerotic plaques. . 2026. PMID 41708636 · DOI · PMC13031644
- Huang Y, Hong W, Wei X. The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis. J Hematol Oncol. 2022. PMID 36076302 · DOI · PMC9461252
- Bakir B, Chiarella AM, Pitarresi JR, Rustgi AK. EMT, MET, Plasticity, and Tumor Metastasis. Trends Cell Biol. 2020. PMID 32800658 · DOI · PMC7647095
- Lin D, Shen L, Luo M, Zhang K, Li J, Yang Q, et al.. Circulating tumor cells: biology and clinical significance. Signal Transduct Target Ther. 2021. PMID 34803167 · DOI · PMC8606574
- Brabletz S, Schuhwerk H, Brabletz T, Stemmler MP. Dynamic EMT: a multi-tool for tumor progression. EMBO J. 2021. PMID 34459003 · DOI · PMC8441439
- Wang Y, Qi H, Liu Y, Duan C, Liu X, Xia T, et al.. The double-edged roles of ROS in cancer prevention and therapy. Theranostics. 2021. PMID 33754031 · DOI · PMC7978298
- Lambert AW, Weinberg RA. Linking EMT programmes to normal and neoplastic epithelial stem cells. Nat Rev Cancer. 2021. PMID 33547455 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.