ArticleCell adhesion & migration
An emerging role for class I bHLH E2-2 proteins in EMT regulation and tumor progression.
Article in Cell adhesion & migration. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Transcription factor 4 is a key mediator of oncogenesis in neuroblastoma by promoting MYC activity.Molecular oncology · 2025Article
- Signaling networks controlling ID and E protein activity in T cell differentiation and function.Frontiers in immunology · 2022Review
- Pitt-Hopkins syndrome: phenotypic and genotypic description of four unrelated patients and structural analysis of corresponding missense mutations.Neurogenetics · 2021Article
- Genetic mutations and molecular mechanisms of Fuchs endothelial corneal dystrophy.Eye and vision (London, England) · 2021Review
- Dihydroartemisinin inhibits the migration of esophageal cancer cells by inducing autophagy.Oncology letters · 2020Article
- EMT Factors and Metabolic Pathways in Cancer.Frontiers in oncology · 2020Review
- Quantitative Studies of Muscleblind Proteins and Their Interaction With TCF4 RNA Foci Support Involvement in the Mechanism of Fuchs' Dystrophy.Investigative ophthalmology & visual science · 2019Article
- The Molecular Basis of Fuchs' Endothelial Corneal Dystrophy.Molecular diagnosis & therapy · 2019Review
- Expression and clinical significance of transcription factor 4 (TCF4) in epithelial ovarian cancer.Cancer biomarkers : section A of Disease markers · 2019Article
- Tumor xenograft modeling identifies an association between TCF4 loss and breast cancer chemoresistance.Disease models & mechanisms · 2018Article
- Ginsenoside Rb1 inhibits hypoxia-induced epithelial-mesenchymal transition in ovarian cancer cells by regulating microRNA-25.Experimental and therapeutic medicine · 2017Article
- CTG18.1 repeat expansion may reduce TCF4 gene expression in corneal endothelial cells of German patients with Fuchs' dystrophy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2017Article
- The Id-protein family in developmental and cancer-associated pathways.Cell communication and signaling : CCS · 2017Review
- Sohlh2 suppresses epithelial to mesenchymal transition in breast cancer via downregulation of IL-8.Oncotarget · 2016Article
- Glucocorticoid Receptor-Targeted Liposomal Codelivery of Lipophilic Drug and Anti-Hsp90 Gene: Strategy to Induce Drug-Sensitivity, EMT-Reversal, and Reduced Malignancy in Aggressive Tumors.Molecular pharmaceutics · 2016Article
- Comprehensive assessment of genetic variants within TCF4 in Fuchs' endothelial corneal dystrophy.Investigative ophthalmology & visual science · 2014Article
- Association and familial segregation of CTG18.1 trinucleotide repeat expansion of TCF4 gene in Fuchs' endothelial corneal dystrophy.Investigative ophthalmology & visual science · 2014Article
- Regulatory networks defining EMT during cancer initiation and progression.Nature reviews. Cancer · 2013Review
- E47 and Id1 interplay in epithelial-mesenchymal transition.PloS one · 2013Article
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
EMT is a complex process whereby cells lose cell-cell interactions and other epithelial properties whilst acquiring a migratory and mesenchymal phenotype. EMT is presently recognized as an important even for tumor invasion and metastasis. Functional E-cadherin loss is a hallmark of EMT and required for tumor invasion in the majority of carcinomas. Transcriptional downregulation is one of the major mechanisms for E-cadherin suppression in carcinomas. In the last decade several E-cadherin repressors, belonging to different transcriptional families, have been identified that, importantly, also act as potent EMT inducers. One of the last additions to EMT regulators are the class I bHLH factors E2-2 (also known as TCF4). However, the hierarchical and functional interrelations between the different EMT inducers are still poorly understood. Here, we comment on the new and so far unrecognized function of E2-2 factors in EMT and discuss on the potential interactions among various EMT inducers. Emerging evidence supporting the participation of TCF4 in human malignancies is also discussed. Thus, increasing understanding of EMT and its regulators is providing meaningful insights into the present knowledge on tumor progression.
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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.