Panoply™ Human CLDN6 Knockdown Stable Cell Line

Claudin 6 (CLDN6), a member of the tight junction family, is involved in intercellular adhesion, acting as a physical barrier to prevent the free passage of solutes and water through the extracellular space. CLDN6 has important biological functions, and its abnormal expression is associated with hepatitis C virus infection. However, limited research has examined its role in gastric cancer. Here, researchers found that CLDN6 mRNA and protein expression is upregulated in gastric cancer cell lines and tissues, indicating a poor prognosis. In vitro and in vivo experiments demonstrated that abnormal CLDN6 expression is associated with enhanced gastric cancer proliferation and invasion. CLDN6 interacts with LATS1/2 in the Hippo signaling pathway, reducing the phosphorylation of LATS1/2 and YAP1, thereby impairing YAP1 nuclear translocation and altering downstream target genes. Furthermore, YAP1 interacts with snail1, affecting the epithelial-mesenchymal transition (EMT) process and enhancing the invasiveness of gastric cancer cells. In summary, CLDN6 promotes gastric cancer proliferation and invasion by affecting YAP1 and the YAP1-snail1 axis.

To further investigate the biological function of CLDN6 in gastric cancer, researchers generated CLDN6 knockdown MKN28 and AGS cell lines and verified knockdown efficiency by quantitative PCR. Colony formation and CCK8 assays revealed that the proliferation of gastric cancer cells was inhibited in CLDN6 knockdown cells (Figure 1a-c). Wound healing and Transwell assays revealed that downregulating CLDN6 expression significantly reduced the migration ability of gastric cancer cells (Figure 1d-g). These results suggest that silencing CLDN6 expression can inhibit the proliferation and invasion of gastric cancer cells in vitro.

Figure 1. CLDN6 promotes proliferation and invasion abilities of GC in vitro. (Yu S, et al., 2019)