ArticleTranslational cancer research2025
KRT23 promotes proliferation invasion and metastasis of gastric cancer through epithelial-mesenchymal transition mediated by the PI3K/AKT/mTOR signaling pathway.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Gastric cancer (GC) is a highly prevalent and lethal malignancy worldwide. Notwithstanding advances in treatment, suboptimal patient outcomes highlight the urgent need for novel therapeutic targets to improve survival. This study aimed to explore the influence of keratin 23 (KRT23) on the proliferation, migration, and invasion of GC cells, as well as its underlying molecular mechanism. Methods: In this research, the correlation between KRT23 expression and prognosis in GC and the sensitivity analysis of chemotherapy drugs were predicted using bioinformatics methods. The expression pattern of KRT23 in GC samples and cells was examined through immunohistochemistry, quantitative polymerase chain reaction (qPCR), and Western blot. Treatments involving KRT23 knockdown in combination with the PI3K activator (740Y-P) and inhibitor (PI3K-IN-1) were employed. The proliferation, migration, and invasion capabilities of GC cells (MGC803/SGC7901) were analyzed via Cell Counting Kit-8 (CCK-8) and Transwell experiments, and the expression of epithelial-mesenchymal transition (EMT) markers and proteins in the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway was detected using Western blot. Results: KRT23 was highly expressed in GC. Knockdown of KRT23 significantly inhibited cell proliferation [short hairpin RNA KRT23 (shKRT23) Conclusions: KRT23 is highly expressed in GC tissues. Knockdown of KRT23 can significantly suppress the proliferation, migration, and invasion of GC cells, and its mechanism might be closely related to the PI3K/AKT/mTOR signaling pathway.
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