ArticleClinics (Sao Paulo, Brazil)2025
CST1 promoted gastric cancer development by activating the AKT pathway.
Article in Clinics (Sao Paulo, Brazil), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Dissecting origin factors of lymph node metastasis in non-small cell lung cancer via multimodal omics.Nature communications · 2026Article
- DDX3 inhibits PTZ-induced ferroptosis in human neuronal SH-SY5Y cells via Wnt/β-catenin signaling.In vitro cellular & developmental biology. Animal · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric Cancer (GC) was the third highest mortality rate among malignant tumors. Currently, no specific treatment is utilized to prevent the progression of GC. The detailed mechanism of GC was still elusive and this study aimed to clarify the mechanism of GC occurrence and development.
methodThis study was performed to clarify the molecular mechanisms of CST1 promoting GC development through activating AKT. The normal gastric tissue cells and GC cell was obtained, followed by transfection with oe-CST1 or sh-CST1, and their apoptosis and viability were evaluated. Finally, Western blot, Flow cytometry assay, Transwell assay, and Scratch assay were used to elucidate the molecular mechanisms of CST1 promoting GC development through activating the AKT pathway.
resultsResearch outcomes show a significant elevation in CST1 and AKT protein as well as mRNA quantities in both the model and CST1-activator cohorts in relation to the control. Conversely, these proteins and mRNA concentrations were notably decreased in the presence of the CST1 inhibitor when compared to the model group, a difference that was statistically significant as evidenced by the p-value.
conclusionCST1 can promote the gastric cancer process by targeting the AKT pathway.
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