ReviewToxicological research2010
Epithelial-mesenchymal Transition and Cell Invasion.
Review in Toxicological research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 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
180 citing papers in PubMed, 324 citations in OpenAlex.
- Suppression of NGALR impedes TNBC cell survival, proliferation, invasion, and migration through Akt/mTOR and JAK/STAT3 pathway inhibition.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- The antifibrotic effects of a click chemistry-based albumin nanocomplex in an idiopathic pulmonary fibrosis model.Journal of nanobiotechnology · 2026Article
- Suppression of Tumor Aggression Through Metabolic Reprogramming via Oxamate Targeting LDHA.International journal of molecular sciences · 2026Review
- Fluoxetine suppresses triple-negative breast cancer progression by inducing apoptosis, inhibiting Src-mediated invasiveness, and enhancing anti-tumor immunity.Molecular medicine (Cambridge, Mass.) · 2026Article
- The effect ofArchives of medical science : AMS · 2026Article
- Phillyrin Modulates AMPK-Associated Cellular Responses and Migration in PC3 Prostate Cancer Cells.Journal of toxicology · 2026Article
- How Traditional Chinese Medicine Works: Biological Mechanisms and Clinical Evidence for Hepatocellular Carcinoma Treatment.Drug design, development and therapy · 2026Review
- Targeting the unfolded protein response in cancer: exploiting endoplasmic reticulum stress for therapeutic intervention.Biochemical pharmacology · 2025Review
- Effects of sesamin on the chemosensitivity, invasiveness and immune evasion mechanism of human lung adenocarcinoma.International journal of molecular medicine · 2025Article
- Epithelial-Immune Cell Crosstalk in Salivary Gland Tumors: Implications for Tumor Progression and Diagnostic Assessment.International journal of molecular sciences · 2025Article
- The T-Box Transcription Factors TBX2 and TBX3 Are Molecular Targets of Piroctone Olamine in the Treatment of Pancreatic Cancer.Journal of cellular and molecular medicine · 2025Article
- Investigating the Effects of ONC206 Alone and in Combination with Cisplatin on Ovarian Cancer Cell Models.Current issues in molecular biology · 2025Article
- Inhibiting SNX10 induces autophagy to suppress invasion and EMT and inhibits the PI3K/AKT pathway in cervical cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Matrix metalloproteinase-driven epithelial-mesenchymal transition: implications in health and disease.Journal of translational medicine · 2025Review
- The proteome of osteoblasts in a 3D culture perfusion bioreactor model compared with static conditions.Scientific reports · 2025Article
- Molecular Dynamics of Breast Cancer Subtypes: The Role of FAM83H-AS1 Long Non-coding RNA in Breast Cancer Metastasis.Breast cancer research and treatment · 2025Article
- The Role of Twisted Gastrulation 1 (TWSG1) Gene in TGF-β Signaling Linked to Cancer: A Comprehensive Review.Asian Pacific journal of cancer prevention : APJCP · 2025Review
- A Boolean network model of hypoxia, mechanosensing and TGF-β signaling captures the role of phenotypic plasticity and mutations in tumor metastasis.PLoS computational biology · 2025Article
- Multiomics Analysis Reveals Molecular Changes during Early Progression of Precancerous Lesions to Lung Adenocarcinoma in Never-Smokers.Cancer research · 2025Article
- Review
120 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a complex process in which epithelial cells acquire the characteristics of invasive mesenchymal cells. EMT has been implicated in cancer progression and metastasis as well as the formation of many tissues and organs during development. Epithelial cells undergoing EMT lose cell-cell adhesion structures and polarity, and rearrange their cytoskeletons. Several oncogenic pathways such as transforming growth factor (TGF) -β, Wnt, and Notch signaling pathways, have been shown to induce EMT. These pathways have activated transcription factors including Snail, Slug, and the ZEB family which work as transcriptional repressors of E-cadherin, thereby making epithelial cells motile and resistant to apoptosis. Mounting evidence shows that EMT is associated with cell invasion and tumor progression.In this review, we summarize the characteristic features of EMT, pathways leading to EMT, and the role of EMT in cell invasion. Three topics are addressed in this review: (1) Definition of EMT, (2) Signaling pathways leading to EMT, (3) Role of EMT in cell invasion. Understanding the role of EMT in cell invasion will provide valuable information for establishing strategies to develop anti-metastatic therapeutics which modulate malignant cellular processes mediated by EMT.
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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.