ArticleScientific reports2025
Kindlin-1 promotes gastric cancer cell motility through the Wnt/β-catenin signaling pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- CRISPR/Cas9-mediated claudin-2 knockout in HCT116 cells reveals its key role in colorectal cancer progression.Oncology letters · 2026Article
- Review
- Nuclear Galectin-1 Drives Cancer Progression throughInternational journal of biological sciences · 2026Article
- Pharmacological inhibition of Ubiquitin-Specific Peptidase 10 (USP10) with spautin-1 attenuates adipogenesis through CCAAT/Enhancer-Binding Protein Beta (C/EBPβ) destabilization.Molecular biomedicine · 2025Article
- Article
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12 authors.
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Abstract
Despite advances in gastric cancer diagnosis and treatment, its prognosis remains poor owing to aggressive tumor progression and metastasis. As understanding the relevant molecular mechanisms is essential to effectively improve patient outcomes, we elucidated the role of Kindlin-1 in gastric cancer progression and metastasis. Kindlin-1 expression was analyzed in 359 gastric cancer tissue samples provided by Kangnam Sacred Heart Hospital and publicly available GSE datasets. Kindlin-1 showed significantly higher expression in gastric cancer tissues than that in normal tissues, and high Kindlin-1 expression was associated with poor prognosis. Further, the mRNA and protein expression of Kindlin-1 were high in gastric cancer cell lines, where they were associated with increased proliferation, migration, and invasion. Our findings demonstrated that Kindlin-1 regulated epithelial-mesenchymal transition-related genes through interaction with activated Wnt/β-catenin signaling. Notably, Kindlin-1 enhanced β-catenin expression and promoted its nuclear translocation from the cytoplasm, increasing TCF4 transcriptional activity and inducing gastric cancer progression and metastasis. Overall, these findings demonstrate that Kindlin-1 is upregulated in gastric cancer and activates Wnt/β-catenin signaling to promote cell proliferation and motility.
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