ArticleGastroenterology2010
Epithelial to mesenchymal transition is impaired in colon cancer cells with microsatellite instability.
Article in Gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 115 citations in OpenAlex.
- CMS4 epithelial-intrinsic glycosyltransferase GALNT5 promotes tumor aggressiveness and correlates with poor survival in colorectal cancer.Scientific reports · 2026Article
- Nanomedicine innovations in colon and rectal cancer: advances in targeted drug and gene delivery systems.Medical oncology (Northwood, London, England) · 2025Review
- POLQ knockdown inhibits proliferation, migration, and invasion by inducing cell cycle arrest in colorectal cancer.Discover oncology · 2024Article
- Association between the expression of epithelial-mesenchymal transition (EMT)-related markers and oncologic outcomes of colorectal cancer.Updates in surgery · 2024Article
- TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer.Heliyon · 2024Article
- Multiomics of Colorectal Cancer Organoids Reveals Putative Mediators of Cancer Progression Resulting from SMAD4 Inactivation.Journal of proteome research · 2023Article
- Five EMT-related genes signature predicts overall survival and immune environment in microsatellite instability-high gastric cancer.Cancer medicine · 2023Article
- Cisplatin-induced activation of TGF-β signaling contributes to drug resistance.Oncology research · 2023Article
- Relationship between Epithelial-to-Mesenchymal Transition and Tumor-Associated Macrophages in Colorectal Liver Metastases.International journal of molecular sciences · 2022Review
- Reliable epithelial-mesenchymal transition biomarkers for colorectal cancer detection.Biomarkers in medicine · 2022Article
- Transforming growth factor-β in tumour development.Frontiers in molecular biosciences · 2022Review
- Epithelial to Mesenchymal Transition: A Challenging Playground for Translational Research. Current Models and Focus onInternational journal of molecular sciences · 2021Review
- Human colorectal cancer-on-chip model to study the microenvironmental influence on early metastatic spread.iScience · 2021Article
- The DDX39B/FUT3/TGFβR-I axis promotes tumor metastasis and EMT in colorectal cancer.Cell death & disease · 2021Article
- TGFβ biology in cancer progression and immunotherapy.Nature reviews. Clinical oncology · 2021Review
- Gastrointestinal Nematode-Derived Antigens Alter Colorectal Cancer Cell Proliferation and Migration through Regulation of Cell Cycle and Epithelial-Mesenchymal Transition Proteins.International journal of molecular sciences · 2020Article
- Mesenchymal subtype neuroblastomas are addicted to TGF-βR2/HMGCR-driven protein geranylgeranylation.Scientific reports · 2020Article
- DSTYK Promotes Metastasis and ChemoresistanceFrontiers in pharmacology · 2020Article
- Transforming Growth Factor-β Signaling Pathway in Colorectal Cancer and Its Tumor Microenvironment.International journal of molecular sciences · 2019Review
- Visualization of epithelial-mesenchymal transition in an inflammatory microenvironment-colorectal cancer network.Scientific reports · 2019Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsColorectal cancers (CRCs) displaying DNA microsatellite instability (MSI) are associated with a favorable natural history, but the molecular basis for this observation has not been defined. We sought to determine whether the epithelial to mesenchymal transition (EMT) is impaired in MSI-positive CRCs that characteristically have a mutant transforming growth factor-beta receptor type II (TGFBR2) gene.
methodsThe induction of EMT by transforming growth factor-beta1 (TGF-beta1) was analyzed by phase contrast microscopy, immunofluorescence, quantitative reverse transcription polymerase chain reaction, immunoblotting, and cellular migration, and invasion assays. Expression of EMT markers was evaluated by immunohistochemistry and quantitative reverse transcription polymerase chain reaction in a series of human colorectal tumors.
resultsTGF-beta1 induced changes in cellular morphology, gene expression, motility, and invasion consistent with EMT in microsatellite stable (MSS) colon cancer cells, whereas cells with MSI and mutant TGFBR2 were unresponsive to TGF-beta1. These effects did not require Smad4, but depended on the recruitment of extracellular signal-regulated kinase. Tumor cells with MSI but wild-type TGFBR2 underwent EMT in response to TGF-beta1, indicating that TGFBR2 genotype is a key determinant of the EMT response in tumors with MSI. In human colorectal tumors, expression of EMT markers was significantly associated with adverse clinicopathologic features and the absence of MSI.
conclusionsThese findings define a unique genotype-phenotype relationship between TGFBR2 and EMT that may contribute to the improved prognosis consistently observed in colon cancers with MSI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.