WIPF1 promotes gastric cancer progression by regulating PI3K/Akt signaling in a myocardin-dependent manner

Wiskott_Aldrich syndrome protein-interacting protein family member 1 (WIPF1) is associated with malignant tumor progression. However, molecular links between WIPF1 and gastric cancer (GC) growth and metastasis remain elusive. WIPF1 was detected in GC tissues and cells in cellular and animal models. The molecular regulatory mechanisms of WIPF1 in GC were explored. WIPF1 was overexpressed in GC tissues and cells and high expression of WIPF1 was an independent risk factor for a poor prognosis in patients with GC.In this study, it was demonstrated that WIPF1 increases the proliferation and migration of GC cells in vitro and promotes GC growth and metastasis in vivo by activating PI3K signaling. Moreover, bioinformatics analysis and subsequent experiments confirmed that myocardin (MYOCD) transactivated WIPF1 expression. Additionally, WIPF1 is necessary for MYOCD to promote the malignant phenotype of GC cells by activating the PI3K signaling pathway, suggesting that the MYOCD axis may contribute to the onset and development of GC.