ArticleThe Journal of biological chemistry2010
Claudin-1 acts through c-Abl-protein kinase Cdelta (PKCdelta) signaling and has a causal role in the acquisition of invasive capacity in human liver cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 122 citations in OpenAlex.
- Claudin proteins as emerging therapeutic targets for solid tumours.Nature reviews. Cancer · 2026Review
- Esculetin Attenuates the Migration and Invasion of Human Hepatocellular Carcinoma Cells by Attenuating Matrix Metalloproteinase Activity and Strengthening Tight Junctions.Journal of cancer prevention · 2025Article
- Hyperplastic ovarian stromal cells express genes associated to tumor progression: a case study.BMC veterinary research · 2024Article
- Expression and Targeted Application of Claudins Family in Hepatobiliary and Pancreatic Diseases.Journal of hepatocellular carcinoma · 2024Review
- Claudins: from gatekeepers of epithelial integrity to potential targets in hepato-pancreato-biliary cancers.Frontiers in oncology · 2024Review
- Expression patterns of claudins in cancer.Heliyon · 2023Review
- Twist1‑mediated transcriptional activation of Claudin‑4 promotes cervical cancer cell migration and invasion.Oncology letters · 2023Article
- Identification and characterization of a first-generation inhibitor of claudin-1 in colon cancer progression and metastasis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Protein Kinase C Delta Is a Novel Biomarker for Hepatocellular Carcinoma.Gastro hep advances · 2023Article
- Role of the ABL tyrosine kinases in the epithelial-mesenchymal transition and the metastatic cascade.Cell communication and signaling : CCS · 2021Review
- Article
- Context-Dependent Roles of Claudins in Tumorigenesis.Frontiers in oncology · 2021Review
- Role of Barrier Integrity and Dysfunctions in Maintaining the Healthy Gut and Their Health Outcomes.Frontiers in physiology · 2021Review
- Tight Junction Proteins and the Biology of Hepatobiliary Disease.International journal of molecular sciences · 2020Review
- Claudin-1, A Double-Edged Sword in Cancer.International journal of molecular sciences · 2020Review
- Tight Junctions in Cell Proliferation.International journal of molecular sciences · 2019Review
- ADAM15 mediates upregulation of Claudin-1 expression in breast cancer cells.Scientific reports · 2019Article
- Immunoreactivity patterns of tight junction proteins are useful for differential diagnosis of human salivary gland tumors.Medical molecular morphology · 2019Article
- Review
- Claudin 1 Is Highly Upregulated by PKC in MCF7 Human Breast Cancer Cells and Correlates Positively with PKCε in Patient Biopsies.Translational oncology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Claudins are identified as members of the tetraspanin family of proteins, which are integral to the structure and function of tight junction. Recent studies showed an increase in expression of claudins during tumorigenesis, which is associated with loss of cell-cell contact, dedifferentiation, and invasiveness. However, the molecular basis for the causal relationship between claudin expression and cancer progression is not fully understood yet. In this study, we show that claudin-1 plays a causal role in the acquisition of invasive capacity in human liver cells and that c-Abl-protein kinase Cdelta (PKCdelta) signaling is critical for the malignant progression induced by claudin-1. Overexpression of claudin-1 clearly induced expression of matrix metalloproteinase-2 (MMP-2) and cell invasion and migration in normal liver cells as well as in non-invasive human hepatocellular carcinoma (HCC) cells. Conversely, small interfering RNA targeting of claudin-1 in invasive HCC cells completely inhibited cell invasion. Both c-Abl and PKCdelta are found to be activated in normal liver cell line clones that stably overexpress claudin-1. Inhibition of either c-Abl or PKCdelta alone clearly attenuated MMP-2 activation and impeded cell invasion and migration in both human HCC and normal liver cells expressing claudin-1. These results indicate that claudin-1 is both necessary and sufficient to induce invasive behavior in human liver cells and that activation of c-Abl-PKCdelta signaling pathway is critically required for the claudin-1-induced acquisition of the malignant phenotype. The present observations raise the possibility of exploiting claudin-1 as a potential biomarker for the spread of liver cancer and might provide pivotal points for therapeutic intervention in HCC.
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