Panoply™ Human PDE4B Over-expressing Stable Cell Line

Bladder cancer (UBC) is a common malignant tumor with a high incidence rate. Advances in the diagnosis and treatment of this disease necessitate the search for novel therapeutic targets. Multiple studies have shown that PDE4B expression is upregulated in malignant tumors, and high PDE4B expression is associated with poor prognosis. Here, researchers have identified PDE4B as a potential therapeutic target for UBC. PDE4B expression is associated with aggressive clinicopathological features and poor prognosis. Functional studies have shown that ectopic PDE4B expression promotes UBC cell proliferation, migration, and invasion, while PDE4B knockdown inhibits cancer cell invasiveness. Researchers also discovered that CBX7 is a regulator of PDE4B, inhibiting its expression at the transcriptional level in a PRC1-dependent manner. Furthermore, these results indicate that PDE4B induces epithelial-mesenchymal transition (EMT) in UBC cells through the β-catenin pathway, and that inhibiting PDE4B using the small molecule inhibitor rolipram effectively reverses the effects induced by PDE4B overexpression. In summary, these results indicate that PDE4B promotes the migration and invasion of UBC cells through the β-catenin/EMT pathway, thereby playing the role of an oncogene.

PDE4B may play an oncogene role in the progression of urothelial carcinoma (UBC). Furthermore, researchers found that PDE4B expression levels were higher in most UBC cell lines than in the non-malignant urothelial cell line SV-HUC-1 (Figure 1A). Interestingly, high PDE4B expression specifically occurred in the basal/squamous cell subtypes, which are precisely the UBC subtypes with poor prognosis. To investigate the potential oncogenic role of PDE4B, researchers stably ectopically expressed PDE4B in T24 cells with relatively low endogenous PDE4B expression (Figures 1A and 1B). First, they explored the effect of PDE4B on cell proliferation. The results showed that PDE4B overexpression significantly improved the survival of T24 cells (Figure 1C). Consistent with this, PDE4B overexpression significantly enhanced the invasiveness of cancer cells (Figures 1D and 1E). Wound healing assays also showed that PDE4B overexpression significantly promoted cell migration (Figures 1F and 1G). In summary, these results indicate that PDE4B overexpression promotes the proliferation and invasion of UBC cells.

Figure 1. Ectopic PDE4B promotes UBC cells proliferation and invasion. (Huang Z, et al., 2021)