MFAP2 promotes the malignant progression of gastric cancer via activating the PI3K/AKT signaling pathway.

Abstract

Gastric cancer (GC) is one of the major cancers of the digestive system, ranking fifth in both incidence and cancer-related mortality worldwide. However, the molecular mechanisms underlying the occurrence and progression of GC remain elusive. By analyzing differentially expressed genes (DEGs) using datasets from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, we identified that MFAP2 mRNA is significantly overexpressed in GC tissues, and higher MFAP2 expression is associated with poorer prognosis in GC patients. Gain- and loss-of-function experiments confirmed that MFAP2 promotes the proliferation of MKN45 using CCK8 assays and colony formation assays. Mechanistically, bioinformatics analysis revealed that MFAP2 could activate the PI3K/AKT signaling pathway, which was further validated by rescue experiments. Finally, we confirmed that MFAP2 also promotes the proliferation of GC cells in vivo by subcutaneous xenograft model in BABL/c mice. Our study provided new insights for the early diagnosis and precision treatment of GC.