ReviewCancer management and research2019
Genetic And Epigenetic Regulation Of E-Cadherin Signaling In Human Hepatocellular Carcinoma.
Review in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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
23 citing papers in PubMed, 42 citations in OpenAlex.
- PSMC2 serves as a potential regulatory target of EZH2 in promoting glioma progression via epithelial-mesenchymal transition.Scientific reports · 2026Article
- DDX39B K63-linked ubiquitination mediated by TRIM28 promotes NSCLC metastasis by enhancing ECAD lysosomal degradation.Signal transduction and targeted therapy · 2025Article
- Unraveling the Role of the Wnt Pathway in Hepatocellular Carcinoma: From Molecular Mechanisms to Therapeutic Implications.Journal of clinical and translational hepatology · 2025Review
- The DNA Methylation is Involved in Liver Cancer Metastasis via Regulation of E- cadherin Gene.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Article
- NSD3 protein methylation and stabilization transforms human ES cells into variant state.Life science alliance · 2025Article
- Article
- Epigenetic modification of hepatitis B virus infection and related hepatocellular carcinoma.Virulence · 2024Review
- Comprehensive review and updated analysis of DNA methylation in hepatocellular carcinoma: From basic research to clinical application.Clinical and translational medicine · 2024Review
- EFNA5 suppresses cell proliferation and tumor metastasis in hepatoma via epithelial-to-mesenchymal transition.Discover oncology · 2024Article
- Molecular Mechanisms in Tumorigenesis of Hepatocellular Carcinoma and in Target Treatments-An Overview.Biomolecules · 2024Review
- Detection of CDH1 gene promoter hypermethylation in gastric cancer and chronic gastritis.Practical laboratory medicine · 2024Article
- Hypoxia disrupt tight junctions and promote metastasis of oral squamous cell carcinoma via loss of par3.Cancer cell international · 2023Article
- Article
- Epithelial-to-Mesenchymal Transition in Metastasis: Focus on Laryngeal Carcinoma.Biomedicines · 2022Review
- Chronic Leptin Treatment Induces Epithelial-Mesenchymal Transition in MCF10A Mammary Epithelial Cells.Journal of mammary gland biology and neoplasia · 2022Article
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- NAFLD exacerbates cholangitis and promotes cholangiocellular carcinoma in mice.Cancer science · 2021Article
- A requirement for p120-catenin in the metastasis of invasive ductal breast cancer.Journal of cell science · 2021Article
- Non-Coding RNAs Set a New Phenotypic Frontier in Prostate Cancer Metastasis and Resistance.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.
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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.