Panoply™ Human FOLR1 Knockdown Stable Cell Line

GBM is an aggressive brain tumor with limited treatment options. Previous studies have implicated FOLR1 as a key gene involved in cancer pathogenesis. Here, researchers investigated the expression pattern of FOLR1 in GBM, its impact on patient prognosis, and its role in GBM cell growth and the SRC/ERK1/2 signaling pathway. The study found that FOLR1 is highly expressed in GBM patients and correlates with poor prognosis. Cell-based experiments demonstrated that FOLR1 overexpression promotes GBM cell growth, whereas low expression of FOLR1 inhibits cell growth. Furthermore, genes associated with FOLR1 are enriched in pathways such as lysosomes and toxoplasmosis. The study further demonstrated that FOLR1 promotes activation of the SRC/ERK1/2 signaling pathway in GBM cells, and attenuation of these pathways effectively inhibits the tumor-promoting effects of FOLR1 in GBM cells. Together, these studies reveal that FOLR1 regulates the malignant progression of GBM by stimulating the SRC/ERK1/2 signaling axis, highlighting its critical role in GBM pathogenesis.

In FOLR1 knockdown U-87 MG and LN-229 cell lines, the researchers observed a significant decrease in FOLR1 expression in GBM cells, which was confirmed by qRT-PCR and WB analysis (Figure 1A). Subsequently, they used CCK-8 experiments, and the results showed that FOLR1 gene downregulation effectively inhibited cell proliferation (Figures 1B and 1C). Transwell experiments showed that FOLR1 gene knockdown significantly reduced cell migration and invasion (Figures 1D and 1E). These results indicate that FOLR1 is an important regulator of GBM cell proliferation, migration, and invasion, and changes in its expression level directly affect the malignancy of GBM. Therefore, FOLR1 is a potential therapeutic target, and new GBM treatment strategies are expected to be developed by regulating FOLR1 or its signaling pathway.

Figure 1. Cellular behavior of FOLR1 knockdown in GBM. (Jia X, et al., 2025)