ArticleOpen life sciences2025
Mechanism of KLF4 Inhibition of epithelial-mesenchymal transition in gastric cancer cells.
Article in Open life sciences, 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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4 authors.
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Abstract
This study investigates the mechanism by which Krüppel-like Factor 4 (KLF4) suppresses epithelial-mesenchymal transition (EMT) in gastric cancer cells. Using Western blot (WB) and reverse transcription-quantitative PCR (RT-qPCR), we evaluated KLF4 protein and mRNA expression levels across gastric cancer cell lines with varying degrees of differentiation. The BGC-823 cell line, which exhibited the lowest KLF4 expression at both protein and mRNA levels, was selected for transfection with a KLF4-overexpressing lentivirus. Following transfection, the Wnt signaling pathway inhibitor XAV-939 and agonist SKL2001 were administered to the KLF4-overexpressing cells. Subsequent Western blot and RT-qPCR analyses were performed to assess the expression of Wnt signaling components and EMT-related markers. Results demonstrated that KLF4 overexpression inhibits EMT in gastric cancer cells through the Wnt/β-catenin signaling pathway. Thus, this study concludes that KLF4 may modulate EMT in gastric cancer cells via the Wnt/β-catenin pathway.
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