Panoply™ Human CSNK1E Knockdown Stable Cell Line

Melanoma (MM) is the deadliest type of skin cancer, originating from melanocytes. Although advances in immunotherapy have improved the prognosis of MM patients to some extent, high levels of drug resistance still lead to poor clinical outcomes. Therefore, identifying new biomarkers and therapeutic targets is crucial for improving the prognosis and treatment of MM. Here, researchers found that CSNK1E and RAC3 were significantly positively correlated with the epithelial-mesenchymal transition (EMT) process, with the expression trend of CSNK1E being similar to that of EMT-related genes. These two genes were also negatively correlated with various immune cell types and immune checkpoint genes. A 13-gene prognostic model showed excellent performance in predicting MM prognosis. Pan-cancer analysis further revealed heterogeneous expression patterns and prognostic potential of CSNK1E in various cancers. Wet lab experiments confirmed that CSNK1E promotes MM cell proliferation, invasion, and migration through the TGF-β signaling pathway and enhances malignant progression. These findings suggest that CSNK1E plays a key role in MM progression and may serve as a potential therapeutic target.

Transwell assay results showed that compared with the control group (NC group), the number of invading and migrating cells was significantly reduced in the CSNK1E knockdown group, further indicating a decrease in their invasion and migration abilities (Figure 1A). In CSNK1E knockdown cells, the protein levels of E-cadherin and ZO1 were significantly increased, while the levels of N-cadherin, vimentin, and MMP9 were significantly decreased (Figure 1B). Immunofluorescence results showed that in CSNK1E knockdown cells, the levels of CSNK1E and vimentin were decreased, while the level of ZO1 was increased (Figure 1C).

Figure 1. Effects of CSNK1E on invasion and migration, along with its influence on related protein expression. (Hong W, et al., 2025)