Panoply™ Human TNFSF4 Over-expressing Stable Cell Line

As a member of the tumor necrosis factor (TNF) superfamily, tumor necrosis factor superfamily member 4 (TNFSF4) is expressed on antigen-presenting cells and activates T cells by binding to its receptor TNFRSF4. However, the tumorigenicity of TNFSF4 has not been studied in a pan-cancer population. Here, researchers performed a comprehensive bioinformatics analysis of the pan-cancer population to explore the mechanism by which TNFSF4 regulates tumorigenesis. Pan-cancer population analysis showed that TNFSF4 was upregulated in multiple tumors. There was also a significant correlation between TNFSF4 expression and single-cell data in multiple cancer types. TNFSF4 expression was associated with the expression of immune checkpoint genes and may affect the sensitivity of multiple drugs. In vitro and in vivo experiments showed that TNFSF4 can promote the occurrence and development of hepatocellular carcinoma (HCC). TNFSF4 is upregulated in multiple cancer types and promotes the occurrence and development of cancer through multiple mechanisms such as regulating tumor infiltration of immune cells. These studies indicate that TNFSF4 is a promising prognostic and immunotherapy biomarker in certain malignancies.

The researchers detected the expression level of TNFSF4 in tumor tissues of 11 HCC patients by qRT-PCR. The results showed that the mRNA level of TNFSF4 in HCC tissues was significantly higher than that in the corresponding normal liver tissues, which was consistent with the results of the TCGA database (Figure 1A). Subsequently, TNFSF4 was overexpressed in Hepa1-6 cells using a plasmid that specifically expressed TNFSF4. Immunostaining results showed that the TNFSF4 overexpression plasmid successfully overexpressed TNFSF4 (Figure 10). The results of the scratch repair experiment, Transwell experiment and clone formation experiment showed that TNFSF4 overexpression promoted the migration, invasion and proliferation of Hepa1-6 cells (Figure 1C-I). In addition, tumor xenograft experiments showed that TNFSF4 overexpression promoted the in vivo growth of Hepa1-6 cells. These results indicate that TNFSF4 promotes the proliferation, invasion and migration of Hepa1-6 cells in vivo and in vitro.

Figure 1. The biological functions of TNFSF4 in HCC. (Deng Z, et al., 2025)