Abstract
PGAM5 has been associated with the development of tumours, however, its function in gastric cancer (GC) remains unexplored. Here, we investigated the role and mechanism of PGAM5 in regulating GC. The results revealed that PGAM5 was upregulated in GC tissues and cell lines, which was correlated with tumour size and TNM stage. Moreover, PGAM5 knockdown inhibited proliferation, migration, and invasion progression, whereas PGAM5 overexpression promoted the function of GC cells in vitro. PGAM5 also promoted the activation of the PI3K/AKT signalling pathway. Furthermore, MK-2206, an AKT inhibitor, reversed the proliferation and activation of the PI3K/AKT signalling pathway induced by PGAM5 knockdown in GC cells. In conclusion, PGAM5 promotes the proliferation of GC by positively regulating the activation of the PI3K/AKT signalling pathway in GC cells.
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