Panoply™ Human KLRB1 Knockdown Stable Cell Line

Lung cancer is the most common primary malignant tumor of the lung. As one of the malignant tumors that poses the greatest threat to human health, its incidence has remained high in recent years. Previous studies have shown that KLRB1 is transcriptionally repressed in lung adenocarcinoma and is associated with the prognosis of lung adenocarcinoma. Here, the researchers explored the intrinsic mechanism by which KLRB1 affects the malignant phenotypes of lung adenocarcinoma, such as immune infiltration, proliferation, growth, and metastasis. Studies have shown that KLRB1 expression in lung cancer tissue is lower than that in surrounding healthy tissue. In the KLRB1 low expression group and high expression group, differentially expressed genes were significantly enriched in immune-related pathways. KLRB1 regulates the growth and proliferation of lung adenocarcinoma cells by affecting the MAPK/ERK signaling pathway. KLRB1 expression is associated with the prognosis, immune infiltration, cell migration and proliferation of lung adenocarcinoma (LUAD).

Here, researchers constructed KLRB1 knockdown A549 cells to examine the role of KLRB1 in lung cancer cells. RT-qPCR and Western blot analysis demonstrated that siRNA suppressed KLRB1 expression in A549 cells (Figures 1A and 1B). The researchers assessed the migration and invasion abilities of control (NC) and KLRB1 knockdown A549 cells. Results showed that KLRB1 knockdown cells significantly enhanced their migration and invasion abilities compared with control cells (Figure 1C). These results suggest that KLRB1 depletion increases the metastatic potential of lung cancer cells in vitro. A CF assay was performed to assess the clonogenicity of KLRB1. Results demonstrated that reduced KLRB1 levels significantly enhanced the CF ability of A549 cells (Figure 1D). CCK-8 analysis demonstrated that KLRB1 knockdown significantly increased A549 cell viability (Figure 1E).

Figure 1. Silencing KLRB1 promoted the migration, invasion and proliferation of lung adenocarcinoma cells in vitro. (Xu S, et al., 2024)