ArticleMolecular biology reports2022
Claudin-6 increases SNAI1, NANOG and SOX2 gene expression in human gastric adenocarcinoma AGS cells.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Involvement of claudins 6 and 9 in epithelial-mesenchymal transition and the metastatic process.Tissue barriers · 2026Review
- The Role of Claudin-1 in Enhancing Pancreatic Cancer Aggressiveness and Drug Resistance via Metabolic Pathway Modulation.Cancers · 2025Article
- Breaking Immunosuppression to Enhance Cancer Stem Cell-Targeted Immunotherapy.International journal of biological sciences · 2025Review
- Possible Strategies to Reduce the Tumorigenic Risk of Reprogrammed Normal and Cancer Cells.International journal of molecular sciences · 2024Review
- Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024Review
- Binding of YY1/CREB to an Enhancer Region Triggers Claudin 6 Expression inInternational journal of molecular sciences · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGastric cancer is a heterogeneous disease associated to deregulated gastric epithelia tight junction barrier function and di novo expression of claudin-6; these changes are associated with epithelial-mesenchymal transition, enhanced invasiveness, metastatic progression, resistance to chemotherapy, and poor prognosis. Gastric cancer stem cells represent a rare population of cells within the tumor implicated in tumor growth and higher tumorigenic capacity. The possible relation between claudin-6 expression and the expression of some markers associated to epithelial mesenchymal transition and cancer stem cells in gastric cancer cells have never been explored. METHODS AND
resultsCD44, CD24, Twist, Villin, DCLK1, claudin-6, NANOG, E-Cadherin, SOX2, and SNAI1 expression was evaluated by immunofluorescence and cytofluorometry in wild type and Claudin-6 transfected AGS cells. Cell migration assays were also performed. Differentially expressed genes and biological processes analysis was performed to determine gene preponderance. The results showed that claudin-6 overexpression enriched the CD44 + /CD24- subpopulation with an overall increase in the expression and the number of CD44 + cells. A significant increase in NANOG, SOX2 and SNAI1 expression and enhanced cell migration was observed in claudin-6 transfected cells. Transcriptome analysis revealed 271 genes involved in enhanced biological processes with only 31 with a significantly p value; thirteen of those genes are closely associated to epithelial mesenchymal transition processes and folding and unfolding processes of proteins in the endoplasmic reticulum.
conclusionsThe pro-tumorigenic effect of claudin-6 in gastric cancer could be associated to dedifferentiation of epithelial cells and an increase in di novo cancer stem cell genesis.
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