Panoply™ Human ICOSLG Knockdown Stable Cell Line

Gastric cancer (GC) has become one of the most common gastrointestinal malignancies. Inducible T-cell costimulatory ligand (ICOSLG) is highly expressed in various cancers and promotes disease progression. Here, researchers aimed to investigate ICOSLG and its potential role in regulating GC cell invasiveness. Results showed that ICOSLG is highly expressed in GC tissues, and GC patients with high ICOSLG expression have a poor prognosis. Furthermore, high ICOSLG levels are associated with higher TNM stage, more lymph node metastasis, and poorer tumor differentiation. ICOSLG knockdown inhibited GC cell proliferation, migration, invasion, and tumor formation, accompanied by decreased glucose consumption, lactate production, and ATP levels. Conversely, ICOSLG overexpression enhanced GC cell invasiveness, an effect that was abrogated by treatment with a glycolysis inhibitor. Further investigation revealed that miR-331–3p is a negative regulator of ICOSLG4; miR-331–3p overexpression reduced ICOSLG4 expression and suppressed the ICOSLG4-induced GC cell invasive phenotype. Taken together, these results suggest that ICOSLG4 is upregulated in gastric cancer cells as an oncogene, promoting glycolysis and a malignant phenotype. MiR-331–3p, which is downregulated in gastric cancer tissues, is a negative regulator of ICOSLG4. Targeting the miR-331–3p/ICOSLG4 axis may inhibit gastric cancer progression.

Here, researchers examined the glycolytic activity of ICOSLG knockdown GC cell lines by analyzing glucose consumption, lactate production, and intracellular ATP levels. Compared with the sh-NC group, ICOSLG knockdown GC cell lines showed significantly reduced intracellular glucose consumption, lactate production, and ATP levels (Figure 1A-C). Therefore, ICOSLG is required for maintaining glycolysis in GC cells.

Figure 1. ICOSLG knockdown inhibits glycolysis in GC cells. (Zhang L, Gao Y. 2024)