ReviewMolecular cancer2016
Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications.
Review in Molecular cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 499 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
499 citing papers in PubMed, 813 citations in OpenAlex.
- Decoding epithelial-mesenchymal transitions with multi-omics.Nature reviews. Genetics · 2026Review
- SNAI2/SLUG: a key regulator of endothelial-to-mesenchymal transition and vascular remodeling in cardiovascular diseases.Journal of cardiothoracic surgery · 2026Review
- Evaluation of Anti-Tumorigenic Effects of Curcumin and Baicalein in 7,12-Dimethylbenz[a] Anthracene-Induced Mammary Gland Tumorigenesis in Wistar Rats.Journal of biochemical and molecular toxicology · 2026Article
- Targeting the Wnt/β-catenin pathway: veratramine mitigates MNNG-induced gastric precancerous lesions.Molecular and cellular biochemistry · 2026Article
- Article
- Regulatory role of IRF2 in proliferation and invasion of nasopharyngeal carcinoma and its underlying mechanism.iScience · 2026Article
- CPS1 promotes colorectal cancer progression by inducing EMT and activating TGF-β/Smad signaling pathway.iScience · 2026Article
- The SP1/NEDD4L Axis Suppresses the Breast Cancer Progression by Downregulating SNAI2 Expression.Biochemical genetics · 2026Article
- Matrix Stiffness Drives Aggressive Phenotype in Tongue Squamous Cell Carcinoma via Mechanotransduction-Stromal Signalling.International dental journal · 2026Article
- Review
- Antitumor effect of dipyridamole mediated by inhibiting the interaction between platelets and tumor cells.Discover oncology · 2026Review
- Review
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- The Role of Oral Pathobionts' Outer Membrane Vesicles in Cancer Pathology and Therapeutic Development.Cells · 2026Review
- Clinicopathological and Prognostic Implications of Epithelial-to-Mesenchymal Transition-Related Immunohistochemical Markers in Resectable Pancreatic Cancer: A Retrospective Longitudinal Study.Cancer reports (Hoboken, N.J.) · 2026Article
- Rewiring miR-22/SNAI1 via CRISPR-based edge editing destabilizes the epithelial phenotype.NPJ systems biology and applications · 2026Article
- Post-transcriptional activation of TGF-β signaling via SMAD mRNA stabilization by EIF4A3 promotes EMT and metastasis in gastric cancer.Cell biology and toxicology · 2026Article
- MiProChip: A Scalable Microfluidic Platform for Multiplexed Single-Cell Proteomics via Isobaric Labeling.Analytical chemistry · 2026Article
- Decoding the regulatory code: O-GlcNAcylation in epithelial-mesenchymal transition (EMT).The Journal of biological chemistry · 2026Review
- Paired-Box (PAX) Gene Signatures as a Biomarker of Breast Cancer Progression.International journal of molecular sciences · 2026Article
439 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial to mesenchymal transition (EMT) is a biological process in which a non-motile epithelial cell changes to a mesenchymal phenotype with invasive capacities. This phenomenon has been well documented in multiple biological processes including embryogenesis, fibrosis, tumor progression and metastasis. The hallmark of EMT is the loss of epithelial surface markers, most notably E-cadherin, and the acquisition of mesenchymal markers including vimentin and N-cadherin. The downregulation of E-cadherin during EMT can be mediated by its transcriptional repression through the binding of EMT transcription factors (EMT-TFs) such as SNAIL, SLUG and TWIST to E-boxes present in the E-cadherin promoter. Additionally, EMT-TFs can also cooperate with several enzymes to repress the expression of E-cadherin and regulate EMT at the epigenetic and post- translational level. In this review, we will focus on epigenetic and post- translational modifications that are important in EMT. In addition, we will provide an overview of the various therapeutic approaches currently being investigated to undermine EMT and hence, the metastatic progression of cancer as well.
Indexed as
Identifiers
What OpenQuestion holds
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.