ArticleOncogene2013
Claudin-1 induces epithelial-mesenchymal transition through activation of the c-Abl-ERK signaling pathway in human liver cells.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 127 papers.
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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
127 citing papers in PubMed, 223 citations in OpenAlex.
- Prognostic relevance and molecular correlates of Claudin-1 expression in pancreatic neuroendocrine tumors.Human pathology · 2026Article
- Claudin proteins as emerging therapeutic targets for solid tumours.Nature reviews. Cancer · 2026Review
- Loss of protein phosphatase 1 regulator TIMAP protein triggers EMT in A549 cells.Cell communication and signaling : CCS · 2026Article
- Crosstalk between TGF-β and Wnt/β-catenin signaling drives fibrogenic and stem-like phenotypes in senescent MDA-MB-231 breast cancer cells.npj aging · 2026Article
- Claudins in ovarian cancer: emerging biomarkers and therapeutic targets.Tissue barriers · 2026Review
- Cancer-testis antigen ACRBP: Cytotoxic response to its HLA-A2 restricted peptide and immune features in ovarian cancer.Human vaccines & immunotherapeutics · 2025Article
- Epithelial to Mesenchymal Transition Transcriptional Regulator ZEB1 in Liver Cancer: Oncogenic Roles and Therapeutic Potential.International journal of molecular sciences · 2025Review
- PABPC3 drives ovarian cancer metastasis and drug sensitivity by downregulating CLDN1 expression.Cell death & disease · 2025Article
- SURF: A Self-Supervised Deep Learning Method for Reference-Free Deconvolution in Spatial Transcriptomics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Role of Claudin-1 in Enhancing Pancreatic Cancer Aggressiveness and Drug Resistance via Metabolic Pathway Modulation.Cancers · 2025Article
- Long-term expansion of basal cells and the novel differentiation methods identify mechanisms for switching Claudin expression in normal epithelia.Scientific reports · 2025Article
- Micro RNA-175 TargetsGenes · 2024Article
- Retraction: CD44 Expression Denotes a Subpopulation of Gastric Cancer Cells in Which Hedgehog Signaling Promotes Chemotherapy Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Indole-3-Acetic Acid Protects Against Lipopolysaccharide-induced Endothelial Cell Dysfunction and Lung Injury through the Activation of USP40.American journal of respiratory cell and molecular biology · 2024Article
- Disabled-2, a versatile tissue matrix multifunctional scaffold protein with multifaceted signaling: Unveiling its potential in the cancer battle.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Regulatory role of Echinochrome A in cancer-associated fibroblast-mediated lung cancer cell migration.Toxicological research · 2024Article
- Exploring Salivary Epithelial Dysfunction in Sjögren's Disease.International journal of molecular sciences · 2024Review
- USP40 promotes hepatocellular carcinoma cell proliferation, migration and stemness by deubiquitinating and stabilizing Claudin1.Biology direct · 2024Article
- Claudins: from gatekeepers of epithelial integrity to potential targets in hepato-pancreato-biliary cancers.Frontiers in oncology · 2024Review
- Expression and Targeted Application of Claudins Family in Hepatobiliary and Pancreatic Diseases.Journal of hepatocellular carcinoma · 2024Review
67 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
- Retracted
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Claudins (CLDNs) are a family of integral membrane proteins central to the formation of tight junctions, structures that are involved in paracellular transport and cellular growth and differentiation, and are critical for the maintenance of cellular polarity. Recent studies have provided evidence that CLDNs are aberrantly expressed in diverse types of human cancers, including hepatocellular carcinomas (HCCs). However, little is known about how CLDN expression is involved in cancer progression. In this study, we show that CLDN1 has a causal role in the epithelial-mesenchymal transition (EMT) in human liver cells, and that the c-Abl-Ras-Raf-1-ERK1/2 signaling axis is critical for the induction of malignant progression by CLDN1. Overexpression of CLDN1 induced expression of the EMT-regulating transcription factors Slug and Zeb1, and thereby led to repression of E-cadherin, β-catenin expression, enhanced expression of N-cadherin and Vimentin, a loss of cell adhesion, and increased cell motility in normal liver cells and HCC cells. In line with these findings, inhibition of either c-Abl or ERK clearly attenuated CLDN1-induced EMT, as evidenced by a reversal of N-cadherin and E-cadherin expression patterns, and restored normal motility. Collectively, these results indicate that CLDN1 is necessary for the induction of EMT in human liver cells, and that activation of the c-Abl-Ras-Raf-1-ERK1/2 signaling pathway is required for CLDN1-induced acquisition of the malignant phenotype. The present observations suggest that CLDN1 could be exploited as a biomarker for liver cancer metastasis and might provide a pivotal point for therapeutic intervention in HCC.
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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.