Panoply™ Human PIK3CD Over-expressing Stable Cell Line

Gastric cancer (GC) is one of the most common solid tumors with the highest morbidity and mortality rates worldwide. Chronic gastritis and the resulting inflammatory microenvironment are major contributing factors to GC development. Here, researchers discovered that PIK3CD, encoding the class IA PI3K catalytic subunit p110δ, is overexpressed in GC, exhibits tumorigenicity, and is associated with the tumor inflammatory microenvironment. Genetic silencing of PIK3CD in GC cells retards proliferation and migration in vitro and tumorigenicity and metastasis in vivo. Conversely, enhanced PIK3CD expression promoted these phenotypes. Furthermore, pharmacological inhibition of PIK3CD reduced the viability and clonogenic capacity of GC cancer cells. More importantly, the transcription of PIK3CD (but not PIK3CA and PIK3CB) is regulated by the pro-inflammatory IL2/JAK3/STAT5 pathway and tumor-infiltrating immune cells (such as lymphocytes). These findings may reveal novel interactions between the tumor inflammatory microenvironment, the IL2/JAK3/STAT5 signaling pathway, and the PI3K/AKT signaling pathway. Targeting PIK3CD may be a promising treatment strategy for gastric cancer.

To further evaluate the function of PIK3CD, researchers constructed PIK3CD-overexpressing gastric cancer cell lines (Figure 1A). CCK8 assay results showed enhanced proliferation in PIK3CD-overexpressing SGC7901, BGC823, and AGS cells (Figure 1B). Transwell migration and scratch assays also confirmed that PIK3CD-overexpressing gastric cancer cells exhibited improved migration (Figures 1C and 1D). These results suggest that PIK3CD overexpression may play a carcinogenic role in gastric cancer.

Figure 1. The effect of ectopic expression of PIK3CD on GC cell proliferation and migration. (Hu Q, et al., 2024)