# Mechanism of KLF4 Inhibition of epithelial-mesenchymal transition in gastric cancer cells

## TL;DR

This study shows how KLF4, a protein, stops cancer cells from becoming more invasive by blocking a specific signaling pathway.

## Contribution

The novel finding is that KLF4 inhibits EMT in gastric cancer cells via the Wnt/β-catenin signaling pathway.

## Key findings

- KLF4 overexpression reduces epithelial-mesenchymal transition in gastric cancer cells.
- The Wnt/β-catenin pathway is involved in KLF4's suppression of EMT.
- XAV-939 and SKL2001 modulate Wnt signaling in KLF4-overexpressing cells.

## 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.