ArticleCellular oncology (Dordrecht, Netherlands)2022
SLC26A9 deficiency causes gastric intraepithelial neoplasia in mice and aggressive gastric cancer in humans.
Article in Cellular oncology (Dordrecht, Netherlands), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Conventional and Novel Approaches to Establishing Mouse Models of Gastric Cancer in the Past, Present, and Potential Post-H. Pylori Infection Era.Biological procedures online · 2026Review
- Genetically engineered mouse models in gastric precancerous lesions research.World journal of gastrointestinal surgery · 2025Review
- The mammalian acid chitinase promotes oncogenic properties of thyroid cancer cells through the JAK2/STAT3 pathway.European thyroid journal · 2025Article
- Precancerous pathways to gastric cancer: a review of experimental animal models recapitulating the correa cascade.Frontiers in cell and developmental biology · 2025Review
- Advances in modeling gastric intestinal metaplasia: a comprehensive review of experimental models and mechanistic insights.Frontiers in oncology · 2025Review
- SLC26A9 in triple-negative breast cancer stem cells: a network pharmacology and molecular modeling study.Frontiers in bioengineering and biotechnology · 2025Review
- Silencing immune-infiltrating biomarker CCDC80 inhibits malignant characterization and tumor formation in gastric cancer.BMC cancer · 2024Article
- Metabolic regulator ERRγ governs gastric stem cell differentiation into acid-secreting parietal cells.Cell stem cell · 2024Article
- SLC26A9 promotes colorectal tumorigenesis by modulating Wnt/β-catenin signaling.Cell death discovery · 2024Article
- Co-expression pattern of SLC transporter genes associated with the immune landscape and clinical outcomes in gastric cancer.Journal of cellular and molecular medicine · 2023Article
- The mechanisms of gastric mucosal injury: focus on initial chief cell loss as a key target.Cell death discovery · 2023Review
- Gastric precancerous lesions:occurrence, development factors, and treatment.Frontiers in oncology · 2023Review
- Role of spasmolytic polypeptide-expressing metaplasia in gastric mucosal diseases.American journal of cancer research · 2023Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundSolute carrier family 26 member (SLC26A9) is a Cl
methodsThe expression patterns of genes related to transport and enzymatic function, proliferation, apoptosis, inflammation, barrier integrity, metaplasia and neoplasia development were studied by immunohistochemistry (IHC), quantitative RT-PCR, in situ hybridization and RNA microarray analysis. SLC26A9 expression and cellular/clinical phenotypes were studied in primary human GC tissues and GC cell lines.
resultsWe found that both complete and parietal cell-selective Slc26a9 deletion in mice caused spontaneous development of gastric premalignant and malignant lesions. Dysregulated differentiation of gastric stem cells in an inflammatory environment, activated Wnt signaling, cellular hyperproliferation, apoptosis inhibition and metaplasia were observed. Analysis of human gastric precancerous and cancerous tissues revealed that SLC26A9 expression progressively decreased from atrophic gastritis to GC, and that downregulation of SLC26A9 was correlated with patient survival. Exogenous expression of SLC26A9 in GC cells induced upregulation of the Cl
conclusionsOur data indicate that SLC26A9 deletion in parietal cells is sufficient to trigger gastric metaplasia and the development of neoplastic lesions. In addition, we found that SLC26A9 expression decreases during human gastric carcinogenesis, and that exogenous SLC26A9 expression in GC cells reduces their malignant behavior.
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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.