Fig. 3: PILRB stimulates the PI3K/AKT signaling pathway in GC cells. | Cell Death & Disease

Fig. 3: PILRB stimulates the PI3K/AKT signaling pathway in GC cells.

From: PILRB potentiates the PI3K/AKT signaling pathway and reprograms cholesterol metabolism to drive gastric tumorigenesis and metastasis

Fig. 3

A KEGG pathway enriched by differently expressed genes influenced by PILRB in AGS. B, C Western blotting analysis detected that PILRB knockdown remarkably inhibited AKT phosphorylation while not affecting MEK and ERK phosphorylation, and PILRB overexpression substantially promoted AKT phosphorylation while not affecting MEK and ERK phosphorylation (B). Wild-type PILRB reversed inhibition of AKT phosphorylation caused by PILRB depletion (C). D Western blotting analysis shows that PI3K/AKT inhibitor GDC-0941 treatment decreased AKT phosphorylation. E, F Cell colony formation assays showed that the proliferation ability of GC cells was significantly inhibited by GDC-0941 treatment in PILRB overexpression GC cells (E) Quantitative analysis (F). G Western blotting analysis showing siAKT treatment decreased AKT expression. H, I Cell colony formation assays showed that the proliferation ability of GC cells was significantly inhibited by siAKT treatment in PILRB overexpression GC cells (H) Quantitative analysis (I).

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